👤 Xuehui Zhang

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Also published as: A-Mei Zhang, Ai Zhang, Ai-Min Zhang, Aiguo Zhang, Aihua Zhang, Aijun Zhang, Aileen Zhang, Ailin Zhang, Aimei Zhang, Aimin Zhang, Aixiang Zhang, Alaina Zhang, Alex R Zhang, Amy L Zhang, An Zhang, An-Qi Zhang, Anan Zhang, Andrew Zhang, Ang Zhang, Anli Zhang, Anqi Zhang, Anwei Zhang, Anying Zhang, Ao Zhang, Bangke Zhang, Bangzhou Zhang, Bao Long Zhang, Bao-Fu Zhang, Bao-Rong Zhang, Baohu Zhang, Baojing Zhang, Baojun Zhang, Baoren Zhang, Baorong Zhang, Baotong Zhang, Bei B Zhang, Bei Zhang, Bei-Bei Zhang, Beiyu Zhang, Ben Zhang, Benjian Zhang, Benyou Zhang, Bi-Tian Zhang, Biao Zhang, Bicheng Zhang, Bikui Zhang, Bin Zhang, Binbin Zhang, Bing Zhang, Bing-Qi Zhang, Bingbing Zhang, Bingkun Zhang, Bingqiang Zhang, Bingxue Zhang, Bingye Zhang, Bixia Zhang, Bo Zhang, Bo-Fei Zhang, Bo-Heng Zhang, Bo-Ya Zhang, Bochuan Zhang, Bofang Zhang, Bohao Zhang, Bohong Zhang, Bohua Zhang, Bojian Zhang, Bolin Zhang, Boping Zhang, Boqing Zhang, Bosheng Zhang, Bowei Zhang, Bowen Zhang, Boxi Zhang, Boxiang Zhang, Boya Zhang, Boyan Zhang, C D Zhang, C H Zhang, C Zhang, Cai Zhang, Cai-Ling Zhang, Caihong Zhang, Caiping Zhang, Caiqing Zhang, Caishi Zhang, Caiyi Zhang, Caiying Zhang, Caiyu Zhang, Can Zhang, Cathy C Zhang, Chan-na Zhang, Chang Zhang, Chang-Hua Zhang, Changhua Zhang, Changhui Zhang, Changjiang Zhang, Changjing Zhang, Changlin Zhang, Changlong Zhang, Changquan Zhang, Changteng Zhang, Changwang Zhang, Channa Zhang, Chao Zhang, Chao-Hua Zhang, Chao-Sheng Zhang, Chao-Yang Zhang, ChaoDong Zhang, Chaobao Zhang, Chaoke Zhang, Chaoqiang Zhang, Chaoyang Zhang, Chaoyue Zhang, Chen Zhang, Chen-Qi Zhang, Chen-Ran Zhang, Chen-Song Zhang, Chen-Xi Zhang, Chen-Yan Zhang, Chen-Yang Zhang, Chenan Zhang, Chenfei Zhang, Cheng Cheng Zhang, Cheng Zhang, Cheng-Lin Zhang, Cheng-Wei Zhang, Chengbo Zhang, Chengcheng Zhang, Chengfei Zhang, Chenggang Zhang, Chengkai Zhang, Chenglong Zhang, Chengnan Zhang, Chengrui Zhang, Chengsheng Zhang, Chengshi Zhang, Chenguang Zhang, Chengwu Zhang, Chengxiang Zhang, Chengxiong Zhang, Chengyu Zhang, Chenhong Zhang, Chenhui Zhang, Chenjie Zhang, Chenlin Zhang, Chenlu Zhang, Chenmin Zhang, Chenming Zhang, Chenrui Zhang, Chenshuang Zhang, Chenxi Zhang, Chenyan Zhang, Chenyang Zhang, Chenyi Zhang, Chenzi Zhang, Chi Zhang, Chong Zhang, Chong-Hui Zhang, Chongguo Zhang, Chonghe Zhang, Chris Zhiyi Zhang, Chu-Yue Zhang, Chuan Zhang, Chuanfu Zhang, Chuankuan Zhang, Chuankuo Zhang, Chuanmao Zhang, Chuantao Zhang, Chuanxin Zhang, Chuanyong Zhang, Chuchu Zhang, Chumeng Zhang, Chun Zhang, Chun-Lan Zhang, Chun-Mei Zhang, Chun-Qing Zhang, Chungu Zhang, Chunguang Zhang, Chunhai Zhang, Chunhong Zhang, Chunhua Zhang, Chunjun Zhang, Chunli Zhang, Chunling Zhang, Chunqing Zhang, Chunxia Zhang, Chunxiang Zhang, Chunxiao Zhang, Chunyan Zhang, Chunying Zhang, Churen Zhang, Chuting Zhang, Chuyue Zhang, Ci Zhang, Claire Y Zhang, Claire Zhang, Clarence K Zhang, Cong Zhang, Congen Zhang, Cuihua Zhang, Cuijuan Zhang, Cuilin Zhang, Cuiping Zhang, Cuiyu Zhang, Cun Zhang, Da Zhang, Da-Qi Zhang, Da-Wei Zhang, Dachuan Zhang, Dadong Zhang, Daguo Zhang, Dai Zhang, Dalong Zhang, Daming Zhang, Dan Zhang, Dan-Dan Zhang, DanDan Zhang, Danfeng Zhang, Danhua Zhang, Danning Zhang, Danyan Zhang, Danyang Zhang, Daolai Zhang, Daoyong Zhang, Dapeng Zhang, David Y Zhang, David Zhang, Dawei Zhang, Daxin Zhang, Dayi Zhang, De-Jun Zhang, Dekai Zhang, Delai Zhang, Deng-Feng Zhang, Dengke Zhang, Deqiang Zhang, Detao Zhang, Deyi Zhang, Deyin Zhang, Di Zhang, Dian Ming Zhang, Dianbo Zhang, Dianzheng Zhang, Ding Zhang, Dingdong Zhang, Dinghu Zhang, Dingkai Zhang, Dingyi Zhang, Dingyu Zhang, Dong Zhang, Dong-Hui Zhang, Dong-Mei Zhang, Dong-Wei Zhang, Dong-Ying Zhang, Dong-cui Zhang, Dong-juan Zhang, Dong-qiang Zhang, Dongdong Zhang, Dongfeng Zhang, Donghua Zhang, Donghui Zhang, Dongjian Zhang, Dongjie Zhang, Donglei Zhang, Dongmei Zhang, Dongsheng Zhang, Dongxin Zhang, Dongyan Zhang, Dongyang Zhang, Dongying Zhang, Donna D Zhang, Donna Zhang, Duo Zhang, Duoduo Zhang, Duowen Zhang, En Zhang, Enhui Zhang, Enming Zhang, Erchen Zhang, F P Zhang, F Zhang, Fa Zhang, Famin Zhang, Fan Zhang, Fang Zhang, Fanghong Zhang, Fangmei Zhang, Fangting Zhang, Fangyuan Zhang, Fei Zhang, Fei-Ran Zhang, Feifei Zhang, Feixue Zhang, Fen Zhang, Feng Zhang, Fengqing Zhang, Fengshi Zhang, Fengshuo Zhang, Fengwei Zhang, Fengxi Zhang, Fengxia Zhang, Fengxu Zhang, Fomin Zhang, Fred Zhang, Fu-Ping Zhang, Fubo Zhang, Fugui Zhang, Fuhan Zhang, Fujun Zhang, Fukang Zhang, Fuming Zhang, Fuqiang Zhang, Fuquan Zhang, Furen Zhang, Fushun Zhang, Fuxing Zhang, Fuyang Zhang, Fuyuan Zhang, G Zhang, G-Y Zhang, Gan Zhang, Gang Zhang, Ganlin Zhang, Gaoxin Zhang, Gary Zhang, Ge Zhang, Geng Zhang, Genglin Zhang, Genxi Zhang, Geyang Zhang, Gong Zhang, Gu Zhang, Guan-Yan Zhang, Guang Zhang, Guang-Qiong Zhang, Guang-Xian Zhang, Guang-Ya Zhang, Guanghui Zhang, Guangji Zhang, Guanglei Zhang, Guangliang Zhang, Guangping Zhang, Guangqiong Zhang, Guangxian Zhang, Guangxin Zhang, Guangye Zhang, Guangyong Zhang, Guangyuan Zhang, Guanqun Zhang, Gui-Ping Zhang, Guicheng Zhang, Guihua Zhang, Guijie Zhang, Guili Zhang, Guiliang Zhang, Guilin Zhang, Guimin Zhang, Guiping Zhang, Guisen Zhang, Guixia Zhang, Guixiang Zhang, Gumuyang Zhang, Guo-Fang Zhang, Guo-Fu Zhang, Guo-Guo Zhang, Guo-Liang Zhang, Guo-Wei Zhang, Guo-Xiong Zhang, Guoan Zhang, Guochao Zhang, Guodong Zhang, Guofang Zhang, Guofeng Zhang, Guofu Zhang, Guoguo Zhang, Guohua Zhang, Guohui Zhang, Guojun Zhang, Guoli Zhang, Guoliang Zhang, Guolong Zhang, Guomin Zhang, Guoming Zhang, Guoping Zhang, Guoqiang Zhang, Guoqing Zhang, Guorui Zhang, Guosen Zhang, Guowei Zhang, Guoxin Zhang, Guoying Zhang, Guozhi Zhang, H D Zhang, H F Zhang, H L Zhang, H P Zhang, H W Zhang, H X Zhang, H Y Zhang, H Zhang, H-F Zhang, Hai Zhang, Hai-Bo Zhang, Hai-Feng Zhang, Hai-Gang Zhang, Hai-Han Zhang, Hai-Liang Zhang, Hai-Man Zhang, Hai-Ying Zhang, Haibei Zhang, Haibing Zhang, Haibo Zhang, Haicheng Zhang, Haifeng Zhang, Haihong Zhang, Haihua Zhang, Haijiao Zhang, Haijun Zhang, Haikuo Zhang, Hailei Zhang, Hailian Zhang, Hailiang Zhang, Hailin Zhang, Hailing Zhang, Hailong Zhang, Hailou Zhang, Haiming Zhang, Hainan Zhang, Haipeng Zhang, Haisan Zhang, Haisen Zhang, Haitao Zhang, Haiwang Zhang, Haiwei Zhang, Haixia Zhang, Haiyan Zhang, Haiyang Zhang, Haiying Zhang, Haiyue Zhang, Han Zhang, Hanchao Zhang, Hang Zhang, Hanqi Zhang, Hanrui Zhang, Hansi Zhang, Hanting Zhang, Hanwang Zhang, Hanwen Zhang, Hanxu Zhang, Hanyin Zhang, Hanyu Zhang, Hao Zhang, Hao-Chen Zhang, Hao-Yu Zhang, Haohao Zhang, Haojian Zhang, Haojie Zhang, Haojun Zhang, Haokun Zhang, Haolin Zhang, Haomin Zhang, Haonan Zhang, Haopeng Zhang, Haoran Zhang, Haotian Zhang, Haowen Zhang, Haoxing Zhang, Haoyu Zhang, Haoyuan Zhang, Haoyue Zhang, Haozheng Zhang, He Zhang, Hefang Zhang, Hejun Zhang, Heng Zhang, Hengming Zhang, Hengrui Zhang, Hengyuan Zhang, Heping Zhang, Hong Zhang, Hong-Jie Zhang, Hong-Sheng Zhang, Hong-Xing Zhang, Hong-Yu Zhang, Hong-Zhen Zhang, Hongbin Zhang, Hongbing Zhang, Hongcai Zhang, Hongfeng Zhang, Hongfu Zhang, Honghe Zhang, Honghong Zhang, Honghua Zhang, Hongjia Zhang, Hongjie Zhang, Hongjin Zhang, Hongju Zhang, Hongjuan Zhang, Honglei Zhang, Hongliang Zhang, Hongmei Zhang, Hongmin Zhang, Hongquan Zhang, Hongrong Zhang, Hongrui Zhang, Hongsen Zhang, Hongtao Zhang, Hongting Zhang, Hongwu Zhang, Hongxia Zhang, Hongxin Zhang, Hongxing Zhang, Hongya Zhang, Hongyan Zhang, Hongyang Zhang, Hongyi Zhang, Hongying Zhang, Hongyou Zhang, Hongyuan Zhang, Hongyun Zhang, Hongzhong Zhang, Hongzhou Zhang, Houbin Zhang, Hu Zhang, Hua Zhang, Hua-Min Zhang, Hua-Xiong Zhang, Huabing Zhang, Huafeng Zhang, Huaiyong Zhang, Huajia Zhang, Huan Zhang, Huan-Tian Zhang, Huanmin Zhang, Huanqing Zhang, Huanxia Zhang, Huanyu Zhang, Huaqi Zhang, Huaqiu Zhang, Huawei Zhang, Huawen Zhang, Huayang Zhang, Huayong Zhang, Huayu Zhang, Hugang Zhang, Huhan Zhang, Hui Hua Zhang, Hui Z Zhang, Hui Zhang, Hui-Jun Zhang, Hui-Wen Zhang, Huibing Zhang, Huifang Zhang, Huihui Zhang, Huijie Zhang, Huijun Zhang, Huili Zhang, Huilin Zhang, Huimao Zhang, Huimin Zhang, Huiming Zhang, Huiping Zhang, Huiqing Zhang, Huiru Zhang, Huiting Zhang, Huixin Zhang, Huiying Zhang, Huiyu Zhang, Huiyuan Zhang, Huize Zhang, Huizhen Zhang, Igor Ying Zhang, J B Zhang, J R Zhang, J Y Zhang, J Zhang, J-Y Zhang, Jamie Zhang, Jason Z Zhang, Jennifer Y Zhang, Jerry Z Zhang, Ji Yao Zhang, Ji Zhang, Ji-Yuan Zhang, Jia Zhang, Jia-Bao Zhang, Jia-Si Zhang, Jia-Su Zhang, Jia-Xuan Zhang, Jiabi Zhang, Jiachao Zhang, Jiachen Zhang, Jiacheng Zhang, Jiahai Zhang, Jiahao Zhang, Jiahe Zhang, Jiajia Zhang, Jiajing Zhang, Jiaming Zhang, Jian Zhang, Jian-Guo Zhang, Jian-Ping Zhang, Jian-Xu Zhang, Jianan Zhang, Jianbin Zhang, Jianbo Zhang, Jianchao Zhang, Jianduan Zhang, Jianeng Zhang, Jianfa Zhang, Jiang Zhang, Jiangang Zhang, Jianghong Zhang, Jianglin Zhang, Jiangmei Zhang, Jiangtao Zhang, Jianguang Zhang, Jianguo Zhang, Jiangyan Zhang, Jianhai Zhang, Jianhong Zhang, Jianhua Zhang, Jianhui Zhang, Jianing Zhang, Jianjun Zhang, Jiankang Zhang, Jiankun Zhang, Jianliang Zhang, Jianling Zhang, Jianmei Zhang, Jianmin Zhang, Jianming Zhang, Jiannan Zhang, Jianping Zhang, Jianqiong Zhang, Jianshe Zhang, Jianting Zhang, Jianwei Zhang, Jianwen Zhang, Jianwu Zhang, Jianxia Zhang, Jianxiang Zhang, Jianxin Zhang, Jianying Zhang, Jianyong Zhang, Jianzhao Zhang, Jiao Zhang, Jiaqi Zhang, Jiasheng Zhang, Jiawei Zhang, Jiawen Zhang, Jiaxin Zhang, Jiaxing Zhang, Jiayan Zhang, Jiayi Zhang, Jiayin Zhang, Jiaying Zhang, Jiayu Zhang, Jiayuan Zhang, Jibin Zhang, Jicai Zhang, Jie Zhang, Jiecheng Zhang, Jiehao Zhang, Jiejie Zhang, Jieming Zhang, Jieping Zhang, Jieqiong Zhang, Jieying Zhang, Jifa Zhang, Jifeng Zhang, Jihang Zhang, Jimei Zhang, Jiming Zhang, Jimmy Zhang, Jin Zhang, Jin-Ge Zhang, Jin-Jing Zhang, Jin-Man Zhang, Jin-Ru Zhang, Jin-Rui Zhang, Jin-Yu Zhang, Jinbiao Zhang, Jinfan Zhang, Jinfang Zhang, Jinfeng Zhang, Jing Jing Zhang, Jing Zhang, Jing-Bo Zhang, Jing-Chang Zhang, Jing-Fa Zhang, Jing-Lve Zhang, Jing-Nan Zhang, Jing-Qiu Zhang, Jing-Zhan Zhang, JingZi Zhang, Jingchuan Zhang, Jingchun Zhang, Jingdan Zhang, Jingdong Zhang, Jingfa Zhang, Jinghui Zhang, Jingjing Zhang, Jinglan Zhang, Jingli Zhang, Jingliang Zhang, Jinglu Zhang, Jingmei Zhang, Jingmian Zhang, Jingning Zhang, Jingping Zhang, Jingqi Zhang, Jingrong Zhang, Jingru Zhang, Jingshuang Zhang, Jingsong Zhang, Jingtian Zhang, Jingting Zhang, Jingwei Zhang, Jingwen Zhang, Jingxi Zhang, Jingxiao Zhang, Jingxuan Zhang, Jingxue Zhang, Jingyao Zhang, Jingyi Zhang, Jingying Zhang, Jingyu Zhang, Jingyuan Zhang, Jingyue Zhang, Jingzhe Zhang, Jinhua Zhang, Jinhui Zhang, Jinjin Zhang, Jinjing Zhang, Jinliang Zhang, Jinlong Zhang, Jinming Zhang, Jinquan Zhang, Jinrui Zhang, Jinsong Zhang, Jinsu Zhang, Jintao Zhang, Jinwei Zhang, Jinxiu Zhang, Jinyi Zhang, Jinying Zhang, Jinyu Zhang, Jinze Zhang, Jinzhou Zhang, Jiqiang Zhang, Jiquan Zhang, Jishou Zhang, Jishui Zhang, Jitai Zhang, Jiuchun Zhang, Jiupan Zhang, Jiuwei Zhang, Jiuxuan Zhang, Jixia Zhang, Jixing Zhang, Jiyang Zhang, Joe Z Zhang, John H Zhang, John Z H Zhang, Joshua Zhang, Joyce Zhang, Juan Zhang, Juan-Juan Zhang, Jue Zhang, Juliang Zhang, Jun Zhang, Jun-Feng Zhang, Jun-Jie Zhang, Jun-Xiao Zhang, Jun-Xiu Zhang, Jun-ying Zhang, June Zhang, Junfeng Zhang, Junhan Zhang, Junhang Zhang, Junhua Zhang, Junhui Zhang, Junjie Zhang, Junjing Zhang, Junkai Zhang, Junli Zhang, Junling Zhang, Junlong Zhang, Junmei Zhang, Junmin Zhang, Junpei Zhang, Junpeng Zhang, Junping Zhang, Junqing Zhang, Junran Zhang, Junru Zhang, Junsheng Zhang, Juntai Zhang, Junwei Zhang, Junxia Zhang, Junxiao Zhang, Junxing Zhang, Junxiu Zhang, Junyan Zhang, Junyi Zhang, Junying Zhang, Junyu Zhang, Junzhi Zhang, Juqing Zhang, K Y Zhang, K Zhang, Kai Zhang, Kai-Jie Zhang, Kai-Qiang Zhang, Kaichuang Zhang, Kaige Zhang, Kaihua Zhang, Kaihui Zhang, Kailin Zhang, Kailing Zhang, Kaiming Zhang, Kainan Zhang, Kaitai Zhang, Kaituo Zhang, Kaiwen Zhang, Kaiyi Zhang, Kan Zhang, Kang Zhang, Kang-Ling Zhang, Kangjun Zhang, Kangning Zhang, Karen Zhang, Ke Zhang, Ke-Wen Zhang, Ke-lan Zhang, Kefen Zhang, Kejia Zhang, Kejian Zhang, Kejin Zhang, Kejun Zhang, Keke Zhang, Keshan Zhang, Kewen Zhang, Keyi Zhang, Keyong Zhang, Keyu Zhang, Kezhong Zhang, Kongyong Zhang, Kui Zhang, Kui-ming Zhang, Kun Zhang, Kunning Zhang, Kunshan Zhang, Kunyi Zhang, Kuo Zhang, L F Zhang, L Zhang, L-S Zhang, Laihong Zhang, Lan Zhang, Lanfang Zhang, Lanju Zhang, Lanjun Zhang, Lanlan Zhang, Lantian Zhang, Lanyue Zhang, Le Zhang, Le-Le Zhang, Lechi Zhang, Lei Zhang, Lei-Lei Zhang, Lei-Sheng Zhang, Leilei Zhang, Leili Zhang, Leitao Zhang, Leiying Zhang, Lele Zhang, Leli Zhang, Leo H Zhang, Li Zhang, Li-Fen Zhang, Li-Jie Zhang, Li-Ke Zhang, Li-ping Zhang, Lian Zhang, Lian-Lian Zhang, Lianbo Zhang, Lianfeng Zhang, Liang Zhang, Liang-Rong Zhang, Liangdong Zhang, Liangliang Zhang, Liangming Zhang, Lianjun Zhang, Lianmei Zhang, Lianqin Zhang, Lianxin Zhang, Libo Zhang, Lichao Zhang, Lichen Zhang, Licheng Zhang, Lichuan Zhang, Licui Zhang, Lida Zhang, Lie Zhang, Lifan Zhang, Lifang Zhang, Liguo Zhang, Lihong Zhang, Lihua Zhang, Lijian Zhang, Lijiao Zhang, Lijie Zhang, Lijuan Zhang, Lijun Zhang, Lilei Zhang, Lili Zhang, Limei Zhang, Limin Zhang, Liming Zhang, Lin Zhang, Lin-Jie Zhang, Lina Zhang, Linan Zhang, Linbo Zhang, Linda S Zhang, Ling Xia Zhang, Ling Zhang, Ling-Yu Zhang, Lingjie Zhang, Lingli Zhang, Lingling Zhang, Lingna Zhang, Lingqiang Zhang, Lingxiao Zhang, Lingyan Zhang, Lingyu Zhang, Lining Zhang, Linjing Zhang, Linli Zhang, Linlin Zhang, Lintao Zhang, Linyou Zhang, Linyuan Zhang, Liping Zhang, Liqian Zhang, Lirong Zhang, Lishuang Zhang, Litao Zhang, Liu Zhang, Liuming Zhang, Liuwei Zhang, Liwei Zhang, Liwen Zhang, Lixia Zhang, Lixing Zhang, Liyan Zhang, Liyi Zhang, Liyin Zhang, Liying Zhang, Liyu Zhang, Liyuan Zhang, Liyun Zhang, Lizhi Zhang, Long Zhang, Longlong Zhang, Longxin Zhang, Longzhen Zhang, Lu Zhang, Lu-Pei Zhang, Lu-Yang Zhang, Luanluan Zhang, Lucia Zhang, Lufei Zhang, Lukuan Zhang, Lulu Zhang, Lun Zhang, Lunan Zhang, Luning Zhang, Luo Zhang, Luo-Meng Zhang, Luoping Zhang, Lupei Zhang, Lusha Zhang, Luwen Zhang, Luyao Zhang, Luyun Zhang, Luzheng Zhang, Lv-Lang Zhang, M H Zhang, M J Zhang, M M Zhang, M Q Zhang, M X Zhang, M Zhang, Man Zhang, Manjin Zhang, Mao Zhang, Maomao Zhang, Mei Zhang, Mei-Fang Zhang, Mei-Ling Zhang, Mei-Qing Zhang, Mei-Ya Zhang, Mei-Zhen Zhang, MeiLu Zhang, Meidi Zhang, Meijia Zhang, Meiling Zhang, Meimei Zhang, Meishan Zhang, Meiwei Zhang, Meixia Zhang, Meixian Zhang, Meiyu Zhang, Melissa C Zhang, Melody Zhang, Meng Zhang, Meng-Jie Zhang, Meng-Wen Zhang, Meng-Ying Zhang, Mengdi Zhang, Mengguo Zhang, Menghao Zhang, Menghuan Zhang, Menghui Zhang, Mengjia Zhang, Mengjie Zhang, Mengliang Zhang, Menglu Zhang, Mengmeng Zhang, Mengmin Zhang, Mengna Zhang, Mengnan Zhang, Mengni Zhang, Mengqi Zhang, Mengqiu Zhang, Mengren Zhang, Mengshi Zhang, Mengxi Zhang, Mengxian Zhang, Mengxue Zhang, Mengying Zhang, Mengyuan Zhang, Mengyue Zhang, Mengzhao Zhang, Mengzhen Zhang, Mi Zhang, Mianzhi Zhang, Miao Zhang, Miao-Miao Zhang, Miaomiao Zhang, Miaoran Zhang, Michael Zhang, Min Zhang, Minfang Zhang, Ming Zhang, Ming-Jun Zhang, Ming-Liang Zhang, Ming-Ming Zhang, Ming-Rong Zhang, Ming-Yu Zhang, Ming-Zhu Zhang, Mingai Zhang, Mingchang Zhang, Mingdi Zhang, Mingfa Zhang, Mingfeng Zhang, Minghang Zhang, Minghao Zhang, Minghui Zhang, Mingjie Zhang, Mingjiong Zhang, Mingjun Zhang, Mingming Zhang, Mingqi Zhang, Mingtong Zhang, Mingxiang Zhang, Mingxiu Zhang, Mingxuan Zhang, Mingxue Zhang, Mingyang A Zhang, Mingyang Zhang, Mingyao Zhang, Mingyi Zhang, Mingying Zhang, Mingyu Zhang, Mingyuan Zhang, Mingyue Zhang, Mingzhao Zhang, Mingzhen Zhang, Minhong Zhang, Minying Zhang, Minyue Zhang, Minzhi Zhang, Minzhu Zhang, Mo Zhang, Mo-Ruo Zhang, Mu Zhang, Muqing Zhang, Muxin Zhang, Muzi Zhang, N Zhang, Na Zhang, Naijin Zhang, Naiqi Zhang, Naisheng Zhang, Naixia Zhang, Nan Yang Zhang, Nan Zhang, Nan-Nan Zhang, Nana Zhang, Nannan Zhang, Nasha Zhang, Ni Zhang, Niankai Zhang, Nianxiang Zhang, Nieke Zhang, Ning Zhang, Ning-Ping Zhang, Ninghan Zhang, Ningkun Zhang, Ningning Zhang, Ningzhen Zhang, Ningzhi Zhang, Nisi Zhang, Nong Zhang, Nu Zhang, P Zhang, Pan Zhang, Pan-Pan Zhang, Panpan Zhang, Pei Zhang, Pei-Weng Zhang, Pei-Zhuo Zhang, PeiFeng Zhang, Peichun Zhang, Peijing Zhang, Peijun Zhang, Peilin Zhang, Peiqin Zhang, Peiwen Zhang, Peiyi Zhang, Peizhen Zhang, Peng Zhang, Peng-Cheng Zhang, Peng-Fei Zhang, Pengbo Zhang, Pengcheng Zhang, Pengfei Zhang, Pengpeng Zhang, Pengwei Zhang, Pengyuan Zhang, Pili Zhang, Ping Zhang, Ping-Fan Zhang, Pingchuan Zhang, Pinggen Zhang, Pingmei Zhang, Pu-Hong Zhang, Pumin Zhang, Q L Zhang, Q Y Zhang, Q Zhang, Q-D Zhang, Qi Zhang, Qi-Ai Zhang, Qi-Lei Zhang, Qi-Min Zhang, QiYue Zhang, Qian Jun Zhang, Qian ZHANG, Qian-Qian Zhang, Qian-Wen Zhang, Qiang Zhang, Qiang-Sheng Zhang, Qiangsheng Zhang, Qiangyan Zhang, Qianhui Zhang, Qianjun Zhang, Qiannan Zhang, Qianqian Zhang, Qianru Zhang, Qiao-Xia Zhang, Qiaofang Zhang, Qiaojun Zhang, Qiaoxuan Zhang, Qifan Zhang, Qiguo Zhang, Qihao Zhang, Qihong Zhang, Qilong Zhang, Qilu Zhang, Qimin Zhang, Qin Zhang, Qing Zhang, Qing-Hui Zhang, Qing-Zhu Zhang, Qingchao Zhang, Qingcheng Zhang, Qingchuan Zhang, Qingfeng Zhang, Qinghong Zhang, Qinghua Zhang, Qingjiong Zhang, Qingjun Zhang, Qingling Zhang, Qingna Zhang, Qingqing Zhang, Qingquan Zhang, Qingrun Zhang, Qingshuang Zhang, Qingtian Zhang, Qingxiu Zhang, Qingxue Zhang, Qingyu Zhang, Qingyue Zhang, Qingyun Zhang, Qinjun Zhang, Qiong Zhang, Qishu Zhang, Qiu Zhang, Qiuting Zhang, Qiuxia Zhang, Qiuyang Zhang, Qiuyue Zhang, Qiwei Zhang, Qiyong Zhang, Quan Zhang, Quan-bin Zhang, Quanfu Zhang, Quanqi Zhang, Quanquan Zhang, Qun Zhang, Qun-Feng Zhang, Qunchen Zhang, Qunfeng Zhang, Qunyuan Zhang, R Zhang, Ran Zhang, Ranran Zhang, Ren Zhang, Renbo Zhang, Renhe Zhang, Renliang Zhang, Renshuai Zhang, Rey M Zhang, Richard Zhang, Rong Zhang, Rong-Kai Zhang, Rongcai Zhang, Rongchao Zhang, Rongguang Zhang, Rongrong Zhang, Rongxin Zhang, Rongxu Zhang, Rongying Zhang, Rongyu Zhang, Ru Zhang, Rugang Zhang, Rui Long Zhang, Rui Xue Zhang, Rui Yan Zhang, Rui Zhang, Rui-Nan Zhang, Rui-Ning Zhang, Rui-fang Zhang, Ruihao Zhang, Ruihong Zhang, Ruikun Zhang, Ruilin Zhang, Ruiling Zhang, Ruimin Zhang, Ruiqi Zhang, Ruiqian Zhang, Ruisan Zhang, Ruixia Zhang, Ruixin Zhang, Ruixue Zhang, Ruiyan Zhang, Ruiyang Zhang, Ruiying Zhang, Ruizhe Zhang, Ruizhi Zhang, Ruizhong Zhang, Rulin Zhang, Run Zhang, Runcheng Zhang, Runxiang Zhang, Runyun Zhang, Runze Zhang, Ruo-Xin Zhang, Ruohan Zhang, Ruoshi Zhang, Ruotian Zhang, Ruoxuan Zhang, Ruoying Zhang, Rusi Zhang, Ruth Zhang, Ruxiang Zhang, Ruxuan Zhang, Ruyi Zhang, S Y Zhang, S Z Zhang, S Zhang, Sai Zhang, Saidan Zhang, Saifei Zhang, Sainan Zhang, Sanbao Zhang, Sen Zhang, Sha Zhang, Shan Zhang, Shan-Shan Zhang, Shanchun Zhang, Shang Zhang, Shangxiong Zhang, Shanhong Zhang, Shanshan Zhang, Shanxiang Zhang, Shao Kang Zhang, Shao Zhang, Shao-Qi Zhang, Shaochuan Zhang, Shaochun Zhang, Shaofei Zhang, Shaofeng Zhang, Shaohua Zhang, Shaojun Zhang, Shaoyang Zhang, Shaozhao Zhang, Shaozhen Zhang, Shasha Zhang, Shen Zhang, Sheng Zhang, Sheng-Dao Zhang, Sheng-Hong Zhang, Sheng-Qiang Zhang, Sheng-Xiao Zhang, Shengchi Zhang, Shengding Zhang, Shengkun Zhang, Shenglai Zhang, Shenglan Zhang, Shenglei Zhang, Shengli Zhang, Shengming Zhang, Shengnan Zhang, Shengye Zhang, Shenqi Zhang, Shenqian Zhang, Shi Zhang, Shi-Han Zhang, Shi-Jie Zhang, Shi-Meng Zhang, Shi-Qian Zhang, Shi-Yao Zhang, ShiSong Zhang, Shichao Zhang, Shihan Zhang, Shijun Zhang, Shikai Zhang, Shilei Zhang, Shimao Zhang, Shining Zhang, Shiping Zhang, Shiqi Zhang, Shiquan Zhang, Shiti Zhang, Shitian Zhang, Shiwen Zhang, Shiwu Zhang, Shiyao Zhang, Shiyi Zhang, Shiyu Zhang, Shiyun Zhang, Shou-Mei Zhang, Shou-Peng Zhang, Shouyue Zhang, Shu Zhang, Shu-Dong Zhang, Shu-Fan Zhang, Shu-Fang Zhang, Shu-Min Zhang, Shu-Ming Zhang, Shu-Yang Zhang, Shu-Zhen Zhang, Shuai Zhang, Shuai-Nan Zhang, Shuaishuai Zhang, Shuang Zhang, Shuangjie Zhang, Shuanglu Zhang, Shuangxin Zhang, Shubing Zhang, Shuchen Zhang, Shucong Zhang, Shuer Zhang, Shuge Zhang, Shuhong Zhang, Shuijun Zhang, Shujun Zhang, Shuli Zhang, Shulong Zhang, Shun Zhang, Shun-Bo Zhang, Shunfen Zhang, Shunming Zhang, Shuo Zhang, Shupeng Zhang, Shuran Zhang, Shurui Zhang, Shushan Zhang, Shuwan Zhang, Shuwei Zhang, Shuxia Zhang, Shuya Zhang, Shuyan Zhang, Shuyang Zhang, Shuye Zhang, Shuyi Zhang, Shuyuan Zhang, Si Zhang, Si-Zhong Zhang, Sibin Zhang, Sifan Zhang, Sihe Zhang, Simeng Zhang, Simin Zhang, Siqi Zhang, Sisi Zhang, Sixue Zhang, Siyuan Zhang, Siyue Zhang, Sizhong Zhang, Song Zhang, Song-Yang Zhang, Songlin Zhang, Songying Zhang, Sophia L Zhang, Stanley Weihua Zhang, Stephen X Zhang, Su Zhang, Sujiang Zhang, Sulin Zhang, Sumei Zhang, Suming Zhang, Suping Zhang, Susie Zhang, Suya Zhang, Suyang Zhang, Suzhen Zhang, T Zhang, Tangjuan Zhang, Tao Zhang, Tao-Lan Zhang, Taojun Zhang, Taoyuan Zhang, Teng Zhang, Tengfang Zhang, Terry Jianguo Zhang, Ti Zhang, Tian Zhang, Tian-Guang Zhang, Tian-Yu Zhang, Tiane Zhang, Tianfeng Zhang, Tianliang Zhang, Tianlong Zhang, Tianpeng Zhang, Tianshu Zhang, Tiantian Zhang, Tianxi Zhang, Tianxiao Zhang, Tianxin Zhang, Tianyang Zhang, Tianye Zhang, Tianyi Zhang, Tianyu Zhang, Tie-mei Zhang, Tiefeng Zhang, Tiehua Zhang, Tiejun Zhang, Ting Ting Zhang, Ting Zhang, Ting-Ting Zhang, Tinghu Zhang, Tingting Zhang, Tingxue Zhang, Tingying Zhang, Tong Xuan Zhang, Tong Zhang, Tong-Cun Zhang, Tongcun Zhang, Tongfu Zhang, Tonghan Zhang, Tonghua Zhang, Tonghui Zhang, Tongran Zhang, Tongshuo Zhang, Tongtong Zhang, Tongwu Zhang, Tongxin Zhang, Tongxue Zhang, Tuo Zhang, Vita Zhang, W G Zhang, W X Zhang, W Zhang, Wancong Zhang, Wang-Dong Zhang, Wangang Zhang, Wangping Zhang, Wanjiang Zhang, Wanjun Zhang, Wannian Zhang, Wanqi Zhang, Wanting Zhang, Wanying Zhang, Wanyu Zhang, Wei Zhang, Wei-Jia Zhang, Wei-Na Zhang, Wei-Yi Zhang, Weibo Zhang, Weichen Zhang, Weifeng Zhang, Weiguo Zhang, Weihua Zhang, Weijian Zhang, Weikang Zhang, Weili Zhang, Weilin Zhang, Weiling Zhang, Weilong Zhang, Weimin Zhang, Weina Zhang, Weipeng Zhang, Weiping J Zhang, Weiqin Zhang, Weisen Zhang, Weiwei Zhang, Weixia Zhang, Weiyi Zhang, Weiyu Zhang, Weizheng Zhang, Weizhou Zhang, Wen Jun Zhang, Wen Zhang, Wen-Hong Zhang, Wen-Jie Zhang, Wen-Jing Zhang, Wen-Xin Zhang, Wen-Xuan Zhang, Wenbin Zhang, Wenbo Zhang, Wenchao Zhang, Wencheng Zhang, Wencong Zhang, Wendi Zhang, Wenguang Zhang, Wenhao Zhang, Wenhong Zhang, Wenhua Zhang, Wenhui Zhang, Wenji Zhang, Wenjia Zhang, Wenjing Zhang, Wenjuan Zhang, Wenjun Zhang, Wenkai Zhang, Wenkui Zhang, Wenli Zhang, Wenlong Zhang, Wenlu Zhang, Wenming Zhang, Wenqian Zhang, Wenru Zhang, Wentao Zhang, Wenting Zhang, Wenwen Zhang, Wenxi Zhang, Wenxiang Zhang, Wenxin Zhang, Wenxue Zhang, Wenya Zhang, Wenyang Zhang, Wenyi Zhang, Wenyuan Zhang, Wenzhong Zhang, Wuhu Zhang, X N Zhang, X X Zhang, X Y Zhang, X Zhang, X-T Zhang, X-Y Zhang, Xi Zhang, Xi'an Zhang, Xi-Feng Zhang, XiHe Zhang, Xia Zhang, Xian Zhang, Xian-Bo Zhang, Xian-Li Zhang, Xian-Man Zhang, Xiang Yang Zhang, Xiang Zhang, Xiangbin Zhang, Xiangfei Zhang, Xianglian Zhang, Xiangsong Zhang, Xiangwu Zhang, Xiangyang Zhang, Xiangyu Zhang, Xiangzheng Zhang, Xianhong Zhang, Xianhua Zhang, Xianjing Zhang, Xianpeng Zhang, Xianxian Zhang, Xiao Bin Zhang, Xiao Min Zhang, Xiao Yu Cindy Zhang, Xiao Zhang, Xiao-Chang Zhang, Xiao-Cheng Zhang, Xiao-Chong Zhang, Xiao-Feng Zhang, Xiao-Hong Zhang, Xiao-Hua Zhang, Xiao-Jun Zhang, Xiao-Lei Zhang, Xiao-Lin Zhang, Xiao-Ling Zhang, Xiao-Meng Zhang, Xiao-Ming Zhang, Xiao-Qi Zhang, Xiao-Qian Zhang, Xiao-Shuo Zhang, Xiao-Wei Zhang, Xiao-Xuan Zhang, Xiao-Yong Zhang, Xiao-Yu Zhang, Xiao-bo Zhang, Xiao-yan Zhang, XiaoLin Zhang, XiaoPing Zhang, XiaoYi Zhang, Xiaobao Zhang, Xiaobiao Zhang, Xiaobo Zhang, Xiaochang Zhang, Xiaochen Zhang, Xiaochun Zhang, Xiaocong Zhang, Xiaocui Zhang, Xiaodan Zhang, Xiaodong Zhang, Xiaofan Zhang, Xiaofang Zhang, Xiaofei Zhang, Xiaofeng Zhang, Xiaogang Zhang, Xiaohan Zhang, Xiaohong Zhang, Xiaohui Zhang, Xiaojia Zhang, Xiaojian Zhang, Xiaojie Zhang, Xiaojin Zhang, Xiaojing Zhang, Xiaojun Zhang, Xiaokui Zhang, Xiaolan Zhang, Xiaolei Zhang, Xiaoli Zhang, Xiaoling Zhang, Xiaolong Zhang, Xiaomei Zhang, Xiaomeng Zhang, Xiaomin Zhang, Xiaoming Zhang, Xiaoning Zhang, Xiaonyun Zhang, Xiaopei Zhang, Xiaopo Zhang, Xiaoqi Zhang, Xiaoqing Zhang, Xiaorong Zhang, Xiaosheng Zhang, Xiaotian Michelle Zhang, Xiaotian Zhang, Xiaotong Zhang, Xiaotun Zhang, Xiaowan Zhang, Xiaowei Zhang, Xiaoxi Zhang, Xiaoxia Zhang, Xiaoxian Zhang, Xiaoxiao Zhang, Xiaoxin Zhang, Xiaoxue Zhang, Xiaoyan Zhang, Xiaoying Zhang, Xiaoyu Zhang, Xiaoyuan Zhang, Xiaoyue Zhang, Xiaoyun Zhang, Xiaozhe Zhang, Xiayin Zhang, Xibo Zhang, Xieyi Zhang, Xijiang Zhang, Xilin Zhang, Xiling Zhang, Ximei Zhang, Xin Zhang, Xin-Hui Zhang, Xin-Xin Zhang, Xin-Yan Zhang, Xin-Ye Zhang, Xin-Yuan Zhang, Xinan Zhang, Xinbao Zhang, Xinbo Zhang, Xincheng Zhang, Xindang Zhang, Xindong Zhang, Xinfeng Zhang, Xinfu Zhang, Xing Yu Zhang, Xing Zhang, Xingan Zhang, Xingang Zhang, Xingcai Zhang, Xingen Zhang, Xinglai Zhang, Xingong Zhang, Xingwei Zhang, Xingxing Zhang, Xingxu Zhang, Xingyi Zhang, Xingyu Zhang, Xingyuan Zhang, Xinhai Zhang, Xinhan Zhang, Xinhe Zhang, Xinheng Zhang, Xinhong Zhang, Xinhua Zhang, Xinjiang Zhang, Xinjing Zhang, Xinjun Zhang, Xinke Zhang, Xinlei Zhang, Xinlian Zhang, Xinlin Zhang, Xinling Zhang, Xinlong Zhang, Xinlu Zhang, Xinmin Zhang, Xinping Zhang, Xinqiao Zhang, Xinquan Zhang, Xinran Zhang, Xinrui Zhang, Xinruo Zhang, Xintao Zhang, Xinwei Zhang, Xinwu Zhang, Xinxin Zhang, Xinyao Zhang, Xinye Zhang, Xinyi Zhang, Xinyu Zhang, Xinyue Zhang, Xiong Zhang, Xiongjun Zhang, Xiongze Zhang, Xipeng Zhang, Xiping Zhang, Xiu Qi Zhang, Xiu-Juan Zhang, Xiu-Li Zhang, Xiu-Peng Zhang, Xiujie Zhang, Xiujun Zhang, Xiulan Zhang, Xiuming Zhang, Xiupeng Zhang, Xiuping Zhang, Xiuqin Zhang, Xiuqing Zhang, Xiuse Zhang, Xiushan Zhang, Xiuwen Zhang, Xiuxing Zhang, Xiuxiu Zhang, Xiuyin Zhang, Xiuyue Zhang, Xiuyun Zhang, Xiuzhen Zhang, Xixi Zhang, Xixun Zhang, Xiyu Zhang, Xu Dong Zhang, Xu Zhang, Xu-Chao Zhang, Xu-Jun Zhang, Xu-Mei Zhang, Xuan Zhang, Xudan Zhang, Xudong Zhang, Xue Zhang, Xue-Ping Zhang, Xue-Qin Zhang, Xue-Qing Zhang, XueWu Zhang, Xuebao Zhang, Xuebin Zhang, Xuefei Zhang, Xueguang Zhang, Xuehai Zhang, Xuehong Zhang, Xuejiao Zhang, Xuejun C Zhang, Xueli Zhang, Xuelian Zhang, Xuelong Zhang, Xueluo Zhang, Xuemei Zhang, Xuemin Zhang, Xueming Zhang, Xuening Zhang, Xueping Zhang, Xueqia Zhang, Xueqian Zhang, Xueqin Zhang, Xueting Zhang, Xuewei Zhang, Xuewen Zhang, Xuexi Zhang, Xueya Zhang, Xueyan Zhang, Xueyi Zhang, Xueying Zhang, Xuezhi Zhang, Xufang Zhang, Xuhao Zhang, Xujun Zhang, Xunming Zhang, Xuting Zhang, Xutong Zhang, Xuxiang Zhang, Y H Zhang, Y L Zhang, Y Y Zhang, Y Zhang, Y-H Zhang, Ya Zhang, Ya-Juan Zhang, Ya-Li Zhang, Ya-Long Zhang, Ya-Meng Zhang, Yachen Zhang, Yadi Zhang, Yadong Zhang, Yafang Zhang, Yafei Zhang, Yafeng Zhang, Yaguang Zhang, Yahua Zhang, Yajie Zhang, Yajing Zhang, Yajun Zhang, Yakun Zhang, Yalan Zhang, Yali Zhang, Yaling Zhang, Yameng Zhang, Yamin Zhang, Yaming Zhang, Yan Zhang, Yan-Chun Zhang, Yan-Ling Zhang, Yan-Min Zhang, Yan-Qing Zhang, Yanan Zhang, Yanbin Zhang, Yanbing Zhang, Yanchao Zhang, Yandong Zhang, Yanfei Zhang, Yanfen Zhang, Yanfeng Zhang, Yang Zhang, Yang-Yang Zhang, Yangfan Zhang, Yanghui Zhang, Yangqianwen Zhang, Yangyang Zhang, Yangyu Zhang, Yanhong Zhang, Yanhua Zhang, Yani Zhang, Yanjiao Zhang, Yanju Zhang, Yanjun Zhang, Yanli Zhang, Yanlin Zhang, Yanling Zhang, Yanman Zhang, Yanmin Zhang, Yanming Zhang, Yanna Zhang, Yannan Zhang, Yanping Zhang, Yanqiao Zhang, Yanquan Zhang, Yanru Zhang, Yanting Zhang, Yanxia Zhang, Yanxiang Zhang, Yanyan Zhang, Yanyi Zhang, Yanyu Zhang, Yao Zhang, Yao-Hua Zhang, Yaodong Zhang, Yaoxin Zhang, Yaoyang Zhang, Yaoyao Zhang, Yaozhengtai Zhang, Yaping Zhang, Yaqi Zhang, Yaru Zhang, Yashuo Zhang, Yating Zhang, Yawei Zhang, Yaxin Zhang, Yaxuan Zhang, Yayong Zhang, Yazhuo Zhang, Ye Zhang, Yefan Zhang, Yeqian Zhang, Yerui Zhang, Yeting Zhang, Yexiang Zhang, Yi J Zhang, Yi Ping Zhang, Yi Zhang, Yi-Chi Zhang, Yi-Feng Zhang, Yi-Ge Zhang, Yi-Hang Zhang, Yi-Hua Zhang, Yi-Min Zhang, Yi-Ming Zhang, Yi-Qi Zhang, Yi-Wei Zhang, Yi-Wen Zhang, Yi-Xuan Zhang, Yi-Yue Zhang, Yi-yi Zhang, YiJie Zhang, YiPei Zhang, Yibin Zhang, Yibo Zhang, Yichen Zhang, Yichi Zhang, Yidan Zhang, Yidong Zhang, Yifan Zhang, Yifang Zhang, Yige Zhang, Yiguo Zhang, Yihan Zhang, Yihang Zhang, Yihao Zhang, Yiheng Zhang, Yihong Zhang, Yihui Zhang, Yijing Zhang, Yikai Zhang, Yikun Zhang, Yili Zhang, Yiliang Zhang, Yilin Zhang, Yimei Zhang, Yimeng Zhang, Yimin Zhang, Yiming Zhang, Yin Jiang Zhang, Yin Zhang, Yin-Hong Zhang, Yina Zhang, Yinci Zhang, Ying E Zhang, Ying Zhang, Ying-Jun Zhang, Ying-Lin Zhang, Ying-Qian Zhang, Yingang Zhang, Yingchao Zhang, Yinghui Zhang, Yingjie Zhang, Yingli Zhang, Yingmei Zhang, Yingna Zhang, Yingnan Zhang, Yingqi Zhang, Yingqian Zhang, Yingyi Zhang, Yingying Zhang, Yingze Zhang, Yingzi Zhang, Yinhao Zhang, Yinjiang Zhang, Yintang Zhang, Yinzhi Zhang, Yinzhuang Zhang, Yipeng Zhang, Yiping Zhang, Yiqian Zhang, Yiqing Zhang, Yiren Zhang, Yirong Zhang, Yitian Zhang, Yiting Zhang, Yiwan Zhang, Yiwei Zhang, Yiwen Zhang, Yixia Zhang, Yixin Zhang, Yiyao Zhang, Yiyi Zhang, Yiyuan Zhang, Yizhe Zhang, Yizhi Zhang, Yong Zhang, Yong-Guo Zhang, Yong-Liang Zhang, Yong-hong Zhang, Yongbao Zhang, Yongchang Zhang, Yongchao Zhang, Yongci Zhang, Yongfa Zhang, Yongfang Zhang, Yongfeng Zhang, Yonggang Zhang, Yonggen Zhang, Yongguang Zhang, Yongguo Zhang, Yongheng Zhang, Yonghong Zhang, Yonghui Zhang, Yongjie Zhang, Yongjiu Zhang, Yongjuan Zhang, Yonglian Zhang, Yongliang Zhang, Yonglong Zhang, Yongpeng Zhang, Yongping Zhang, Yongqiang Zhang, Yongsheng Zhang, Yongwei Zhang, Yongxiang Zhang, Yongxing Zhang, Yongyan Zhang, Yongyun Zhang, You-Zhi Zhang, Youjin Zhang, Youmin Zhang, Youti Zhang, Youwen Zhang, Youyi Zhang, Youying Zhang, Youzhong Zhang, Yu Chen Zhang, Yu Zhang, Yu-Bo Zhang, Yu-Chi Zhang, Yu-Fei Zhang, Yu-Hui Zhang, Yu-Jie Zhang, Yu-Jing Zhang, Yu-Qi Zhang, Yu-Qiu Zhang, Yu-Yu Zhang, Yu-Zhe Zhang, YuHang Zhang, YuHong Zhang, Yuan Zhang, Yuan-Wei Zhang, Yuan-Yuan Zhang, Yuanchao Zhang, Yuanhao Zhang, Yuanhui Zhang, Yuanping Zhang, Yuanqiang Zhang, Yuanqing Zhang, Yuansheng Zhang, Yuanxi Zhang, Yuanxiang Zhang, Yuanyi Zhang, Yuanyuan Zhang, Yuanzhen Zhang, Yuanzhuang Zhang, Yubin Zhang, Yucai Zhang, Yuchao Zhang, Yuchen Zhang, Yuchi Zhang, Yue Zhang, Yue-Bo Zhang, Yue-Ming Zhang, Yuebin Zhang, Yuebo Zhang, Yuehong Zhang, Yuehua Zhang, Yuejuan Zhang, Yuemei Zhang, Yueqi Zhang, Yueru Zhang, Yuetong Zhang, Yufang Zhang, Yufeng Zhang, Yuhan Zhang, Yuhao Zhang, Yuheng Zhang, Yuhua Zhang, Yuhui Zhang, Yujia Zhang, Yujiao Zhang, Yujie Zhang, Yujin Zhang, Yujing Zhang, Yujuan Zhang, Yuke Zhang, Yukun Zhang, Yulin Zhang, Yuling Zhang, Yulong Zhang, Yumei Zhang, Yumeng Zhang, Yumin Zhang, Yun Zhang, Yun-Feng Zhang, Yun-Lin Zhang, Yun-Mei Zhang, Yun-Sheng Zhang, Yun-Xiang Zhang, Yunfan Zhang, Yunfei Zhang, Yunfeng Zhang, Yunhai Zhang, Yunhang Zhang, Yunhe Zhang, Yunhui Zhang, Yuning Zhang, Yunjia Zhang, Yunli Zhang, Yunmei Zhang, Yunpeng Zhang, Yunqi Zhang, Yunqiang Zhang, Yunqing Zhang, Yunsheng Zhang, Yunxia Zhang, Yupei Zhang, Yupeng Zhang, Yuping Zhang, Yuqi Zhang, Yuqing Zhang, Yurou Zhang, Yuru Zhang, Yusen Zhang, Yushan Zhang, Yutian Zhang, Yuting Zhang, Yutong Zhang, Yuwei Zhang, Yuxi Zhang, Yuxia Zhang, Yuxin Zhang, Yuxuan Zhang, Yuyan Zhang, Yuyanan Zhang, Yuyang Zhang, Yuying Zhang, Yuyu Zhang, Yuyuan Zhang, Yuzhe Zhang, Yuzhi Zhang, Yuzhou Zhang, Yuzhu Zhang, Yvonne Zhang, Z Zhang, Z-K Zhang, Zai-Rong Zhang, Zaifeng Zhang, Zaijun Zhang, Zaiqi Zhang, Zebang Zhang, Zekun Zhang, Zemin Zhang, Zeming Zhang, Zeng Zhang, Zengdi Zhang, Zengfu Zhang, Zenglei Zhang, Zengli Zhang, Zengqiang Zhang, Zengrong Zhang, Zengtie Zhang, Zepeng Zhang, Zewei Zhang, Zewen Zhang, Zeyan Zhang, Zeyuan Zhang, Zhan-Xiong Zhang, Zhangjin Zhang, Zhanhao Zhang, Zhanjie Zhang, Zhanjun Zhang, Zhanming Zhang, Zhanyi Zhang, Zhao Zhang, Zhao-Huan Zhang, Zhao-Ming Zhang, Zhaobo Zhang, Zhaocong Zhang, Zhaofeng Zhang, Zhaohua Zhang, Zhaohuai Zhang, Zhaohuan Zhang, Zhaohui Zhang, Zhaomin Zhang, Zhaoping Zhang, Zhaoqi Zhang, Zhaotian Zhang, Zhaoxue Zhang, Zhe Zhang, Zhehua Zhang, Zhemei Zhang, Zhen Zhang, Zhen-Dong Zhang, Zhen-Jie Zhang, Zhen-Shan Zhang, Zhen-Tao Zhang, Zhen-lin Zhang, Zhenfeng Zhang, Zheng Zhang, Zhengbin Zhang, Zhengfen Zhang, Zhenglang Zhang, Zhengliang Zhang, Zhengxiang Zhang, Zhengxing Zhang, Zhengyu Zhang, Zhengyun Zhang, Zhenhao Zhang, Zhenhua Zhang, Zhenlin Zhang, Zhenqiang Zhang, Zhentao Zhang, Zhenyang Zhang, Zhenyu Zhang, Zhenzhen Zhang, Zhenzhu Zhang, Zhewei Zhang, Zhewen Zhang, Zheyuan Zhang, Zhezhe Zhang, Zhi Zhang, Zhi-Chang Zhang, Zhi-Jie Zhang, Zhi-Jun Zhang, Zhi-Peng Zhang, Zhi-Qing Zhang, Zhi-Shuai Zhang, Zhi-Shuo Zhang, Zhi-Xin Zhang, Zhibo Zhang, Zhicheng Zhang, Zhicong Zhang, Zhifei Zhang, Zhigang Zhang, Zhiguo Zhang, Zhihan Zhang, Zhihao Zhang, Zhihong Zhang, Zhihua Zhang, Zhihui Zhang, Zhijian Zhang, Zhijiao Zhang, Zhijing Zhang, Zhijun Zhang, Zhikun Zhang, Zhimin Zhang, Zhiming Zhang, Zhiping Zhang, Zhiqian Zhang, Zhiqiang Zhang, Zhiqiao Zhang, Zhiru Zhang, Zhishang Zhang, Zhishuai Zhang, Zhiwang Zhang, Zhiwen Zhang, Zhixia Zhang, Zhixin Zhang, Zhiyan Zhang, Zhiyao Zhang, Zhiye Zhang, Zhiyi Zhang, Zhiyong Zhang, Zhiyu Zhang, Zhiyuan Zhang, Zhiyun Zhang, Zhizhong Zhang, Zhong Zhang, Zhong-Bai Zhang, Zhong-Yi Zhang, Zhong-Yin Zhang, Zhong-Yuan Zhang, Zhongheng Zhang, Zhongjie Zhang, Zhonglin Zhang, Zhongqi Zhang, Zhongwei Zhang, Zhongxin Zhang, Zhongxu Zhang, Zhongyang Zhang, Zhongyi Zhang, Zhou Zhang, Zhu Zhang, Zhu-Qin Zhang, Zhuang Zhang, Zhuo Zhang, Zhuo-Ya Zhang, Zhuohua Zhang, Zhuojun Zhang, Zhuorong Zhang, Zhuoya Zhang, Zhuqin Zhang, Zhuqing Zhang, Zhuzhen Zhang, Zi-Feng Zhang, Zi-Jian Zhang, Zian Zhang, Zicheng Zhang, Ziding Zhang, Ziguo Zhang, Zihan Zhang, Ziheng Zhang, Zijian Zhang, Zijiao Zhang, Zijing Zhang, Zikai Zhang, Zilong Zhang, Zilu Zhang, Ziping Zhang, Ziqi Zhang, Zishuo Zhang, Zixiong Zhang, Zixu Zhang, Zixuan Zhang, Ziyang Zhang, Ziyi Zhang, Ziyin Zhang, Ziyu Zhang, Ziyue Zhang, Zizhen Zhang, Zongping Zhang, Zongquan Zhang, Zongwang Zhang, Zongxiang Zhang, Zu-Xuan Zhang, Zufa Zhang, Zuoyi Zhang
articles

The spectrum and prognosis of Sjögren's syndrome with membranous nephropathy.

Dan-Dan Qiu, Zhi Li, Jing-Jing Wang +7 more · 2025 · Clinical kidney journal · Oxford University Press · added 2026-04-24
This study aims to investigate the spectrum and prognosis of membranous nephropathy (MN) in patients with Sjögren's syndrome (SS). SS patients with biopsy-proven kidney involvement who were diagnosed Show more
This study aims to investigate the spectrum and prognosis of membranous nephropathy (MN) in patients with Sjögren's syndrome (SS). SS patients with biopsy-proven kidney involvement who were diagnosed at our center between April 2007 and February 2024 were retrospectively reviewed and analyzed. A total of 290 SS patients with kidney involvement were enrolled. The frequency of MN increased from 16.28% during the 2007-2010 period to 44.05% during the 2021-2024 period. After 2016, MN became the most common renal pathologic type, surpassing tubulointerstitial nephritis. PLA2R antibody or antigen was detected in 74 SS-MN patients, in whom 37 (50%) showed a negative result. Within the PLA2R-negative group, five out of 15 showed positivity for EXT1/EXT2 antigen and one out of eight for THSD7A antigen. Sixty-one SS patients with MN were followed up for >6 months, and 44 (72.13%) of them achieved renal complete remission (CR). Compared with PLA2R-negative patients, PLA2R-positive patients spent a longer time to achieve CR (1.46 ± 1.16 vs. 0.74 ± 0.47 years, MN has become the predominant renal pathologic type in SS. PLA2R-positivity testing followed by EXT1/EXT2 and THSD7A testing is recommended for SS-MN patients. Although most patients can achieve renal CR, the prognosis is usually poor in PLA2R-positive SS-MN patients. Show less
📄 PDF DOI: 10.1093/ckj/sfae384
EXT1

Serum BDNF helps identify favorable subgroups in HCC patients treated with PD-L1 inhibitors and anti-angiogenic TKIs.

Caifeng Gong, Jinglong Huang, Dandan Cao +10 more · 2025 · Therapeutic advances in medical oncology · SAGE Publications · added 2026-04-24
Immune checkpoint inhibitors (ICIs) combined with antiangiogenic agents have become a standard strategy for advanced hepatocellular carcinoma (HCC). There remains an urgent need for effective biomarke Show more
Immune checkpoint inhibitors (ICIs) combined with antiangiogenic agents have become a standard strategy for advanced hepatocellular carcinoma (HCC). There remains an urgent need for effective biomarkers to guide treatment, with C-reactive protein and alpha-fetoprotein in immunotherapy (CRAFITY) scores and cytokine levels representing promising candidates. We aimed to assess the efficacy, safety, and potential biomarkers of anlotinib plus TQB2450 in patients with advanced HCC. This study was a single-arm, phase Ib trial. Twenty-five patients with advanced HCC were enrolled. Patients received an intravenous infusion of TQB2450 (1200 mg, on Day 1) and oral administration of anlotinib (initiated at 10 mg, once a day, from Day 1 to Day 14), which was repeated every 3 weeks. Blood was collected at baseline for serum cytokine analysis. After a median follow-up of 41.80 months, the median progression-free survival (mPFS) was 5.49 months, and the median overall survival (mOS) was 8.94 months. Treatment-related adverse events (TRAEs) occurred in 22 patients, with grade ⩾3 TRAEs observed in 12 patients. Patients who achieved clinical benefit (CB) had higher baseline serum brain-derived neurotrophic factor (BDNF) levels than non-CB patients (median, 227.97 vs 129.26 pg/ml, Anlotinib plus TQB2450 demonstrated promising efficacy with manageable safety in advanced HCC. Elevated serum BDNF levels might serve as a potential positive prognostic marker and, together with ECOG score, may help complement the CRAFITY score in identifying subgroups that could benefit from ICIs and antiangiogenic therapy. Show less
📄 PDF DOI: 10.1177/17588359251407052
BDNF

Preliminary exploration of potential biomarkers for heart failure and bipolar disorder: an exploratory study based on bioinformatics.

Wei Zhang, Na Li · 2025 · Frontiers in psychiatry · Frontiers · added 2026-04-24
Individuals with bipolar disorder (BD) exhibit a significantly increased risk of cardiovascular disease, yet the specific mechanisms linking heart failure (HF) and BD remain poorly understood. This st Show more
Individuals with bipolar disorder (BD) exhibit a significantly increased risk of cardiovascular disease, yet the specific mechanisms linking heart failure (HF) and BD remain poorly understood. This study aimed to identify common potential diagnostic biomarkers associated with both conditions. Differentially expressed genes (DEGs) were analyzed separately in HF (GSE57338) and BD (GSE5389) datasets. Key module genes for each condition were identified through co-expression network analysis and intersected with DEGs to pinpoint candidate genes. Subsequently, a protein-protein interaction (PPI) network, receiver operating characteristic (ROC) analysis, and expression validation were employed to identify potential diagnostic biomarkers. Gene set enrichment analysis (GSEA) and drug predictions were also conducted. Clinical validation of biomarker expression was performed via quantitative polymerase chain reaction (qPCR). A total of 44 candidate genes were identified as being associated with both HF and BD. Six potential diagnostic biomarkers ( This study preliminarily explored the common molecular mechanisms between HF and BD, and identified 6 potential biomarkers for early detection, providing a solid theoretical basis for future research on HF and BD. Show less
📄 PDF DOI: 10.3389/fpsyt.2025.1627105
EXT1

LRRK2 G2019S mutation contributes to mitochondrial transfer dysfunction in a Drp1-STX17-dependent manner.

Mei Ding, Fen Wang, Lan-Lan Jiang +11 more · 2025 · Translational neurodegeneration · BioMed Central · added 2026-04-24
Previous studies have shown that astrocytes can transfer healthy mitochondria to dopaminergic (DA) neurons, which may serve as an intrinsic neuroprotective mechanism in Parkinson's disease (PD). LRRK2 Show more
Previous studies have shown that astrocytes can transfer healthy mitochondria to dopaminergic (DA) neurons, which may serve as an intrinsic neuroprotective mechanism in Parkinson's disease (PD). LRRK2 G2019S is the most common pathogenic mutation associated with PD. In this study, we explored whether mitochondrial transfer is influenced by genetic and environmental factors and whether dysfunction in this process is one of the mechanisms of the pathogenic LRRK2 G2019S mutation. DA neurons and astrocytes were differentiated from induced pluripotent stem cells generated from the peripheral blood of a healthy individual and a PD patient carrying the LRRK2 G2019S mutation. A coculture system of astrocytes and DA neurons was established to explore the pathogenic mechanisms of LRRK2 G2019S. Exposure to the environmental toxin rotenone impaired mitochondrial transfer from astrocytes to DA neurons. Compared with the co-culture system from the healthy participant, the co-culture system harboring the LRRK2 G2019S mutation experienced more pronounced damage. Specifically, STX17 was colocalized with the mitochondrial outer membrane marker TOM20, and its knockdown caused damage to mitochondrial transfer. Drp1 interacted with STX17. LRRK2 G2019S-mutant astrocytes exhibited markedly increased phosphorylation of Drp1 at Ser616 upon rotenone exposure. Moreover, the degree of colocalization of STX17 with TOM20 decreased. The Drp1 phosphorylation inhibitor DUSP6 restored the colocalization of STX17 and TOM20, as well as the mitochondrial transfer efficiency and neuronal survival. The impairment of mitochondrial transfer is a potential pathogenic mechanism associated with LRRK2 G2019S mutation. The molecular mechanisms of mitochondrial transfer were observed to occur through a Drp1-STX17-dependent pathway. Notably, inhibitors for Drp1 Ser616 phosphorylation may offer neuroprotection through mitigating mitochondrial transfer impairments. This study provides novel insights into the pathogenesis of PD and the development of new therapeutic targets. Show less
📄 PDF DOI: 10.1186/s40035-025-00525-1
DUSP6

Inhibition of LPL suppresses the osteoclast differentiation of bone-marrow-derived macrophages by promoting the ACSL4 ubiquitination.

Yansheng Huang, Sibo Wang, Dong Hu +2 more · 2025 · International immunopharmacology · Elsevier · added 2026-04-24
The imbalance between osteoblast (OB) -led bone formation and osteoclast (OC) -induced bone resorption is a recognized reason of osteoporosis. However, further gene-related pathogenesis remains to be Show more
The imbalance between osteoblast (OB) -led bone formation and osteoclast (OC) -induced bone resorption is a recognized reason of osteoporosis. However, further gene-related pathogenesis remains to be elucidated. The microarray profile GSE225974 was used to identify the differentially expressed genes (DEGs) between OC and peripheral blood mononuclear cells (PBMC). Bone-marrow-derived macrophages (BMMs) treated with 30 ng/ml macrophage-colony-stimulating factor (M-CSF) and 100 ng/ml receptor activator of NF-kappa B ligand (RANKL) was to induce osteoclastic differentiation in vitro. The expression of lipoprotein lipase (LPL) was measured by quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting methods. Meanwhile, the regulatory role of LPL on osteoclastic differentiation was evaluated by monitoring cathepsin K levels and TRAP staining. Proteins related to LPL were obtained by STRING, and the interaction between proteins was verified by immunoprecipitation (IP) and ubiquitination analysis. LPL was markedly up-expressed in OCs. Inhibition of LPL suppressed osteoclast differentiation of BMMs by inhibiting cathepsin K and number of TRAP-positive cells. Then the results of STRING demonstrated that proteins related to LPL including the lipid synthesis gene ACSL4. Erastin treatment prominently weakened the effects of si-LPL on cathepsin K levels and TRAP staining intensity by activating ferroptosis. Mechanically, inhibition of LPL suppressed osteoclast differentiation by promoting ubiquitination levels of ACSL4, and over-expression of USP14 reversed the effects of LPL knockdown on regulating ubiquitination of ACSL4. Suppression of LPL inhibits the osteoclast differentiation of BMMs in vitro. The mechanism may be related to the LPL knockdown induced USP14 meidated the ACSL4 ubiquitination. Taken together, down-regulation of LPL may be a promising method to suppress osteoclast differentiation to treat osteoporosis. Show less
no PDF DOI: 10.1016/j.intimp.2025.114694
LPL

Case Report: Two cases of non-small cell lung cancer with coexistence of

Yuping Zhang, Hengming Zhang, Xiufeng Li · 2025 · Frontiers in oncology · Frontiers · added 2026-04-24
To investigate the clinical and pathological characteristics of patients with non-small cell lung cancer exhibiting coexistence of Clinical data, as well as histopathological, immunohistochemical, and Show more
To investigate the clinical and pathological characteristics of patients with non-small cell lung cancer exhibiting coexistence of Clinical data, as well as histopathological, immunohistochemical, and molecular pathological characteristics, of two patients harboring both Both patients were women aged 57 and 66 years. The two cases were diagnosed as invasive lung adenocarcinoma, and immunohistochemical staining showed that all tumor cells expressed CK7, Napsin A, TTF-1, and PD-L1. In Case 1, an Show less
📄 PDF DOI: 10.3389/fonc.2025.1664782
FGFR1

Branched-chain amino acid and cancer: metabolism, immune microenvironment and therapeutic targets.

Hao Xiong, Ruiqi Liu, Keke Xu +7 more · 2025 · Journal of translational medicine · BioMed Central · added 2026-04-24
Cancer is one of the major diseases threatening human health in the world. According to the latest global cancer statistics from the International Agency for Research on Cancer (IARC), there were appr Show more
Cancer is one of the major diseases threatening human health in the world. According to the latest global cancer statistics from the International Agency for Research on Cancer (IARC), there were approximately 20 million new cancer cases and 10 million cancer deaths worldwide. Amidst this global health concern, branched chain amino acids have emerged as key players, playing an important role in the occurrence and development of cancer. In certain malignancies like colorectal cancer, the average level of BCAA in tumor tissues is twice that in normal tissues. BCAA metabolism is intricately associated with the progression of multiple tumors and is modulated by diverse enzymes, including BCAT, BCKDH, and BCKDK. The metabolism of BCAA involves multiple enzymes and biochemical processes via signaling pathways such as PI3K/AKT/mTOR and AMPK/mTOR, etc. In addition, mTOR inhibitors show potential value in cancer treatment by regulating the metabolism and signaling pathways of tumor cells, which provides a new direction for anticancer efforts. Simultaneously, BCAAs are closely associated with tumor immunity, including NK cells, CD4 Show less
📄 PDF DOI: 10.1186/s12967-025-06664-3
BCKDK

Genome-wide transcriptome analysis reveal the molecular mechanism for triggering the formation of purple leaves in rice mutants

Chengyu Wang, Hongyu Zhao, Yujie Zhou +10 more · 2025 · Frontiers in plant science · Frontiers · added 2026-04-24
The color of rice leaves are important agronomic traits that directly influence the proportion of sunlight energy utilization and ultimately affect the yield and quality, so it is crucial to excavate Show more
The color of rice leaves are important agronomic traits that directly influence the proportion of sunlight energy utilization and ultimately affect the yield and quality, so it is crucial to excavate the mechanism of regulating rice leave color. To investigate the molecular mechanism that triggers the purple color in rice leaf, phenotypic characterization and genome-wide transcriptome analysis were conducted using the japonica rice cultivar nipponbare (Nip) and its two purple leaf mutants, A total of 2247, 5484, 4525, 2103, 4375 and7029DEGs (differentially expressed genes) were identified in nip-a vs These results not only revealed the molecular mechanism triggering leaf purple color in the rice mutants Show less
📄 PDF DOI: 10.3389/fpls.2025.1584423
LPL

Targeted intervention in obesity-associated atrial fibrosis using nanoparticle-loaded fusion protein.

Changying Wang, Xiaodong Zhang, Guangwei Zeng · 2025 · Apoptosis : an international journal on programmed cell death · Springer · added 2026-04-24
The association between obesity and atrial fibrillation (AF) has garnered increasing attention. Obesity is a significant risk factor for cardiovascular diseases and promotes the occurrence of AF throu Show more
The association between obesity and atrial fibrillation (AF) has garnered increasing attention. Obesity is a significant risk factor for cardiovascular diseases and promotes the occurrence of AF through multiple mechanisms. This study aims to explore the molecular mechanisms of obesity-induced AF using GLP-1R/GIPR dual-target agonist fusion protein (Fc) loaded into adipose-derived mesenchymal stem cell (ADSC) exosome-liposome hybrid nanoparticles (LE@Fc NPs). We successfully constructed and purified the Fc, verifying its purity and functional activity through SDS-PAGE and UV absorption spectroscopy. The fusion protein was then loaded into nanovesicles, and their morphology, size, and stability were assessed using transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and dynamic light scattering (DLS). In vitro experiments demonstrated that LE@Fc NPs exhibit high fusion efficiency and targeted delivery capability. In vivo experimental results show that LE@Fc NPs significantly inhibit ferroptosis in the epicardial adipose tissue (EAT) of obese mice (iron content: 3.69 ± 0.36 vs. 0.88 ± 0.09), by restoring GSH levels (0.45 ± 0.08 vs. 0.87 ± 0.08) and Gpx4 expression (0.32 ± 0.06 vs. 1.01 ± 0.16), and reducing ROS (12.01 ± 0.95 vs. 2.68 ± 0.17), MDA (3.17 ± 0.29 vs. 0.95 ± 0.09), and 4-HNE (3.74 ± 0.51 vs. 0.91 ± 0.09) levels. Furthermore, LE@Fc NPs treatment significantly improved the inflammatory response (IL-1β: 44.08 ± 3.74 vs. 12.07 ± 0.65, IL-6: 515.59 ± 47.70 vs. 288.43 ± 16.81, MCP-1: 1401.04 ± 194.88 vs. 600.28 ± 45.54, TNF-α: 39.96 ± 2.48 vs. 18.01 ± 0.85). LE@Fc NPs also reduced atrial fibrosis, thereby effectively lowering the incidence of AF. Echocardiography and electrocardiogram monitoring revealed that LE@Fc NPs treatment significantly improved atrial remodeling and reduced the occurrence of AF in obese mice. In addition, LE@Fc NPs significantly improved obesity-induced systemic inflammation and metabolic disorders. In conclusion, LE@Fc NPs show great potential for the treatment of obesity-related AF. Show less
📄 PDF DOI: 10.1007/s10495-025-02104-1
GIPR

Lipoprotein(a), ABO Blood Types and Clinical Outcomes: Novel Findings and Clinical Implications in Patients With Chronic Coronary Syndrome.

Hui-Hui Liu, Chen-Xi Song, Sha Li +12 more · 2025 · MedComm · Wiley · added 2026-04-24
This study aimed to investigate the effect of lipoprotein(a) (Lp(a)) on major adverse cardiovascular events (MACEs) among individuals with chronic coronary syndrome (CCS) according to ABO blood groups Show more
This study aimed to investigate the effect of lipoprotein(a) (Lp(a)) on major adverse cardiovascular events (MACEs) among individuals with chronic coronary syndrome (CCS) according to ABO blood groups. Two independent cohorts of patients with CCS were included consecutively. Blood groups and Lp(a) levels were measured. Patients with the AB group were excluded due to the small sample size. In the exploratory cohort ( Show less
📄 PDF DOI: 10.1002/mco2.70505
LPA

Rational Design and Identification of ISM7594 as a Tissue-Agnostic FGFR2/3 Inhibitor.

Yazhou Wang, Jinxin Liu, Yihong Zhang +14 more · 2025 · Journal of medicinal chemistry · ACS Publications · added 2026-04-24
The selective inhibition of fibroblast growth factor receptors (FGFR) presents a significant challenge due to the high degree of sequence and the close structural similarity of the subtypes. Herein, w Show more
The selective inhibition of fibroblast growth factor receptors (FGFR) presents a significant challenge due to the high degree of sequence and the close structural similarity of the subtypes. Herein, we designed selective dual FGFR2/3 inhibitors based on the in-depth understanding of protein-ligand interaction contributions. We efficiently identified ISM7594 ( Show less
no PDF DOI: 10.1021/acs.jmedchem.5c00928
FGFR1

Elevated BACE1 and IFNγ+ T Cells in Patients with Cognitive Impairment and the 5xFAD Mouse Model.

Yaxi Zhan, Zuolong Chen, Shuxin Zheng +6 more · 2025 · ACS chemical neuroscience · ACS Publications · added 2026-04-24
The dysregulation of T cell differentiation was associated with cognitive impairment. Recently, the peripheric β-secretase (BACE1) has been suggested as a regulator of T cell differentiation, which wa Show more
The dysregulation of T cell differentiation was associated with cognitive impairment. Recently, the peripheric β-secretase (BACE1) has been suggested as a regulator of T cell differentiation, which was increased in both cognitive impairment (CI) and type 2 diabetes mellitus (T2DM) in CI patients. However, the relationship between T cell dysfunction and CI remains unclear. To address this question, we measured T cell subtypes and BACE1 enzyme activity in a clinical cohort and 5xFAD mice. We found that both IFNγ+ Th1 and Tc1 cells were increased in the CI and T2DM-CI groups, which were associated with worsening cognitive function. The elevated IFNγ + Th1 and Tc1 cells were also observed in 8-month-old 5xFAD mice. The elevated BACE1-mediated INSR cleavage was associated with increased IFNγ + Th1 and Tc1 cells. These findings demonstrate the potential role of elevated BACE1 in IFNγ+ T cells and CI. Show less
📄 PDF DOI: 10.1021/acschemneuro.4c00565
BACE1

Heterogeneity of Myocardial Fibrosis Found in Twins With the MYBPC3 Variant Manifesting as Hypertrophic Cardiomyopathy.

Keyan Wang, Haiyu Li, Yong Zhang +2 more · 2025 · Circulation. Cardiovascular imaging · added 2026-04-24
no PDF DOI: 10.1161/CIRCIMAGING.124.017837
MYBPC3

Ginsenoside reprogramming microglia through the FGF/FGFR1 inhibits post traumatic stress disorder.

Huangao Zhou, Hao Pan, Xiangwei Li +4 more · 2025 · International immunopharmacology · Elsevier · added 2026-04-24
Post traumatic stress disorder (PTSD) is a serious and persistent mental diseases. Nowadays, Treatment of PTSD patients in clinical practice is mainly based on drug therapy accompanied by psychologica Show more
Post traumatic stress disorder (PTSD) is a serious and persistent mental diseases. Nowadays, Treatment of PTSD patients in clinical practice is mainly based on drug therapy accompanied by psychological therapy. However, the therapeutic effect is unsatisfactory. It is urgent to detect how to treat PTSD patients. Here, we found that ginsenoside can significantly relieve PTSD symptoms in mice model. Rg3, one of the main pharmacological components of ginsenoside, prevents PTSD by promoting alternatively activated M2 phenotype microglia while inhibiting classically activated inflammatory M1 phenotype microglia. Mechanistically, Rg3 up-regulates fibroblast growth factor receptor 1 (FGFR1) expression in microglia to suppress excessive activation of microglia and reduce neuronal apoptosis. Importantly, knocking down FGFR1 expression in BV2 cells promoted a pro-inflammatory phenotype of BV2 cells, while over-expressing FGFR1 reversed this effect. In vivo PTSD mice model results showed that knockdown FGFR1 prevents the therapeutic effect of Rg3, which indicates that FGFR1 is an essential target of PTSD. Our results reveal that Rg3 may be a potential drug to treat PTSD patients. Show less
no PDF DOI: 10.1016/j.intimp.2024.113763
FGFR1

Therapeutic effect and potential mechanism of Fufang Danshen dripping pills for stable coronary heart disease: a randomized controlled trial.

Li-Qin Meng, Pei-Ying Huang, Qing-Min Li +7 more · 2025 · Frontiers in cardiovascular medicine · Frontiers · added 2026-04-24
The efficacy and mechanism of Fufang Danshen dripping pills (FFDS) in the secondary prevention of stable coronary heart disease (SCHD) is currently undetermined. This study aims to investigate the eff Show more
The efficacy and mechanism of Fufang Danshen dripping pills (FFDS) in the secondary prevention of stable coronary heart disease (SCHD) is currently undetermined. This study aims to investigate the efficacy and preliminary mechanism by which FFDS may impact the progression of SCHD. Based on randomization, we administered oral FFDS to 30 patients with SCHD in addition to conventional treatment for 30 days. After treatment, three-months major adverse cardiovascular events (MACE) were assessed as the primary outcome. Additionally, we evaluated the patients' Seattle Angina Questionnaire score, blood pressure, circulating levels of total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, C-reactive protein, platelets, alanine aminotransferase, aspartate aminotransferase, serum creatinine, and fasting blood glucose as the secondary outcomes. Furthermore, we utilized mass spectrometry analysis, network pharmacology, and lipidomics to predict the potential mechanisms of FFDS in the treatment of SCHD. Following treatment, FFDS demonstrated significant improvements in serum triglyceride levels ( In individuals with SCHD, the administration of FFDS has been shown to effectively reduce circulating triglyceride levels and decrease the frequency of angina episodes. This therapeutic effect is likely due to the active components of FFDS targeting key proteins: LPL, CD36, FABPpm, L-FABP, LCAT, and CEPT. https://www.chictr.org.cn/, identifier (ChiCTR2400080149). Show less
📄 PDF DOI: 10.3389/fcvm.2025.1506917
LPL

Quantitative proteomic analysis reveals potential serum diagnostic markers for colorectal adenoma.

Chengli Yu, Xin Huang, Yating Cao +7 more · 2025 · Frontiers in molecular biosciences · Frontiers · added 2026-04-24
Colorectal cancer (CRC) is one of the leading causes of cancer-related death, and most CRCs arise from colorectal adenomas. Early detection and removal of precancerous lesions during the adenoma-carci Show more
Colorectal cancer (CRC) is one of the leading causes of cancer-related death, and most CRCs arise from colorectal adenomas. Early detection and removal of precancerous lesions during the adenoma-carcinoma sequence can significantly reduce CRC risk. However, current clinical practice lacks rapid, noninvasive screening tools for reliable adenoma detection. Proteomic analysis was performed on serum samples from patients with inflammatory polyps (non-neoplastic), patients with adenomas, and healthy controls to identify key differentially expressed proteins capable of distinguishing adenoma patients. The alterations in these candidate proteins were further validated by ELISA to evaluate their potential as diagnostic biomarkers for colorectal adenoma. In two independent cohorts, we identified two candidate biomarkers, apolipoprotein A4 (APOA4) and filamin A (FLNA), through a multi-step selection process involving ANOVA p-value screening, sparse partial least squares discriminant analysis (sPLS-DA), and LASSO regression analysis. These candidates were subsequently validated in a third cohort using ELISA. The ELISA results for APOA4 were discordant with the liquid chromatography-tandem mass spectrometry (LC-MS/MS) findings. In contrast, FLNA levels measured by ELISA showed a progressive decrease from healthy controls to patients with inflammatory polyps and further to those with adenomas. We propose FLNA as a potential biomarker for the diagnosis of colorectal adenomas. The areas under the ROC curves exceeded 0.7 for both key clinical comparisons: 0.810 for adenomas versus healthy controls, and 0.734 for adenomas versus inflammatory polyps. Overall, this study not only enhances our understanding of the serum proteome in colorectal adenoma but also identifies FLNA as a promising biomarker for its clinical diagnosis. Show less
📄 PDF DOI: 10.3389/fmolb.2025.1628587
APOA4

Accelerometer-measured intensity-specific physical activity, genetic susceptibility, and back pain risk: a UK biobank cohort study.

Yuanpeng Zhu, Di Liu, Xiangjie Yin +3 more · 2025 · The spine journal : official journal of the North American Spine Society · Elsevier · added 2026-04-24
Current clinical guidelines lack clear, quantitative recommendations on intensity-specific physical activity (PA) levels for preventing back pain. Moreover, accelerometer-based evidence regarding dose Show more
Current clinical guidelines lack clear, quantitative recommendations on intensity-specific physical activity (PA) levels for preventing back pain. Moreover, accelerometer-based evidence regarding dose-response relationships and interactions between PA and genetic susceptibility remains limited. To determine the relationships between accelerometer-measured total and intensity-specific PA and incident back pain, and to assess potential effect modification by polygenic risk scores (PRS). Prospective, large-scale, population-based study using UK Biobank data. UK Biobank participants who wore wrist accelerometers for 7 days (N=71,601). Incident back pain, defined as the first recorded ICD-10 dorsalgia code (M54). Total PA, light PA (LPA), and moderate-to-vigorous PA (MVPA) were derived using validated machine-learning algorithms from raw accelerometer data. Dose-response relationships were modeled using restricted cubic splines within Cox proportional hazards models, with adjustment for and stratification by a polygenic risk score (PRS). Point estimates for the population attributable fraction (PAF) were then calculated. Body mass index (BMI) mediation was assessed. Over a median follow-up of 7.0 years, total PA and MVPA exhibited nonlinear inverse associations with incident back pain, independent of genetic risk, with thresholds at approximately 35 milli-g (total PA) and 60 min/day (MVPA). The adjusted PAF was 15.9% for low MVPA and 9.9% for low total PA. Associations were strongest for MVPA, followed by total PA; no significant association was observed for LPA. Within both PRS strata, risk declined monotonically across PA quartiles, with similar effect sizes and no PA × PRS interaction. Notably, participants with high PRS and high PA had lower risk than those with low PRS and low PA. BMI mediated 26.2% of the total PA association and 15.5% of the MVPA association. Accelerometer-measured MVPA robustly reduces back-pain risk, independent of genetic predisposition. Future guidelines should provide clear, intensity-specific recommendations and account for the observed nonlinear dose-response to optimize prevention. Show less
no PDF DOI: 10.1016/j.spinee.2025.10.021
LPA

GPR45 modulates Gα

Yu Xun, Yiao Jiang, Baijie Xu +7 more · 2025 · Science (New York, N.Y.) · Science · added 2026-04-24
The melanocortin system centrally regulates energy homeostasis, with key components such as melanocortin-4 receptor (MC4R) and adenylyl cyclase 3 (ADCY3) in neuronal primary cilia. Mutations in
📄 PDF DOI: 10.1126/science.adp3989
ADCY3

Branched-chain amino acids induce hyperammonemia via gut-liver axis-mediated ammonia overproduction in laying hens.

Huafeng Jian, Mengru Xu, Fang Liu +5 more · 2025 · Animal nutrition (Zhongguo xu mu shou yi xue hui) · Elsevier · added 2026-04-24
Gut microbiota not only biosynthesizes branched-chain amino acids (BCAA) but also catabolizes and utilizes them, while the effects of dietary BCAA supplementation on intestinal microbiota and metaboli Show more
Gut microbiota not only biosynthesizes branched-chain amino acids (BCAA) but also catabolizes and utilizes them, while the effects of dietary BCAA supplementation on intestinal microbiota and metabolism remain largely elusive. Therefore, the present study aimed to investigate the impacts of dietary BCAA supplementation on productive performance, egg quality, gut microbiota and metabolism in laying hens. A total of 180 Fengda No.1 laying hens aged 41 weeks were randomly assigned to five groups, with each group consisting of six replicates of six hens, and the experiment lasted for 8 weeks. The control group (Ctrl AA) was fed a basal diet, while the other four groups were supplemented with 67% leucine (High Leu), isoleucine (High Ile), both leucine and isoleucine (High Leu + Ile), or a combination of the three BCAA (High BCAA), respectively, based on the Ctrl AA. The results demonstrated that compared with Ctrl AA, both High Ile and High BCAA significantly decreased egg mass and laying rate ( Show less
📄 PDF DOI: 10.1016/j.aninu.2025.03.012
CPS1

Establishment of an induced pluripotent stem cell line (HMUCPi001-A) from a hypertrophic cardiomyopathy patient carrying MYBPC3 c.3072C > A mutation.

Dongping Liu, Mingyu Yang, Shasha Fan +6 more · 2025 · Stem cell research · Elsevier · added 2026-04-24
Hypertrophic cardiomyopathy (HCM) is an inherited cardiovascular disorder characterized by left ventricular hypertrophy and an elevated risk of sudden cardiac death. Cardiac myosin binding protein C ( Show more
Hypertrophic cardiomyopathy (HCM) is an inherited cardiovascular disorder characterized by left ventricular hypertrophy and an elevated risk of sudden cardiac death. Cardiac myosin binding protein C (MYBPC3) is the most frequently mutated gene leading to HCM. In this study, peripheral blood mononuclear cells isolated from an HCM patient harboring a heterozygous MYBPC3 missense mutation (c.3072C > A; p.S1024R) were reprogrammed via Sendai virus vectors to generate a patient-specific induced pluripotent stem cell (iPSC) line. The iPSC line exhibits normal morphology and karyotype, alongside definitive hallmarks of pluripotency, including trilineage differentiation potential. Show less
no PDF DOI: 10.1016/j.scr.2025.103841
MYBPC3

Combined network pharmacology and metabolomics reveal that Rubia cordifolia L. ameliorates exhaustive exercise-induced myocardial injury in rats via the BCAA degradation pathway.

Xueyu Niu, Jia Deng, Yan Zhao +4 more · 2025 · Fitoterapia · Elsevier · added 2026-04-24
Rubia cordifolia L. (RCL) is a widely used medicinal with a long history. It exhibits anti-inflammatory and antioxidant properties and prevents apoptosis. While there is growing evidence that exhauste Show more
Rubia cordifolia L. (RCL) is a widely used medicinal with a long history. It exhibits anti-inflammatory and antioxidant properties and prevents apoptosis. While there is growing evidence that exhausted exercise (EE) might cause cardiac damage, RCL has been shown to provide cardioprotective effects. The effects and mechanisms of RCL on exercise-induced myocardial injury remain unclear. In this study, we tested the RCL extract using a rat model of exhausted swimming. We evaluated the therapeutic effect of RCL on exercise-induced myocardial damage using PCR, ELISA, hematoxylin-eosin (H&E) staining, DHE staining, and other methods. UPLC-Q-TOF-MS was employed to identify the components of the RCL extract and its blood-entry components, and network pharmacology was constructed. LC-MS was utilized to investigate left ventricular metabolomics. These two approaches were combined to predict the possible metabolic pathways regulated by RCL. Finally, the targets of the metabolic pathway were verified using molecular docking and western blot analysis. The findings suggest that rubioncolin B, 4-hydroxy-2-carbexyanthraquinone, and 9-Oxo-9H-xanthene-4-carboxylic acid may be the primary active compounds of RCL. RCL promotes the degradation pathway of branched-chain amino acids (BCAA), including valine, leucine, and isoleucine, regulates the proteins BCAT2 and BCKDK, reduces pathological injuries, inflammation, oxidative stress, and collagen deposition, and mitigates the effects of exhaustion-induced myocardial injuries by influencing the key target AKR1C1 and the metabolite L-Valine. This study provides a foundation for the development of RCL as a sports supplement to alleviate EE-induced myocardial injury. Show less
no PDF DOI: 10.1016/j.fitote.2025.106617
BCKDK

Nano-functionalized probiotic treats atherosclerosis via inhibiting intestinal microbiota-TMA-TMAO axis.

Zhezhe Chen, Qiongjun Zhu, Hong Xu +8 more · 2025 · Nature communications · Nature · added 2026-04-24
Many patients are suffering from atherosclerosis without typical risk factors, which can cause severe cardiovascular complications. Trimethylamine N-oxide (TMAO), derived from gut microbes, is a key u Show more
Many patients are suffering from atherosclerosis without typical risk factors, which can cause severe cardiovascular complications. Trimethylamine N-oxide (TMAO), derived from gut microbes, is a key unconventional contributor to the development of atherosclerosis. Here we present a strategy performed by orally administered nano-functionalized probiotics (PDMF@LGG) to inhibit TMAO through the gut microbiota-trimethylamine (TMA)-TMAO axis. PDMF@LGG, composed of polydopamine-coated Lacticaseibacillus rhamnosus GG and nanoparticles based on a reactive oxygen species (ROS)-responsive polymeric prodrug of fluoromethylcholine (FMC), can promote the retention of probiotics and nanoparticles in the intestine to persistently scavenge elevated ROS and release drugs. This process suppresses TMA production and absorption, lowering plasma TMAO levels. The therapeutic effects on male ApoE Show less
📄 PDF DOI: 10.1038/s41467-025-66448-7
APOE

D-Ala2-GIP (1-30) promotes angiogenesis by facilitating endothelial cell migration via the Epac/Rap1/Cdc42 signaling pathway.

Tuchen Guan, Wenxue Zhang, Mingxuan Li +11 more · 2025 · Cellular signalling · Elsevier · added 2026-04-24
Angiogenesis, a meticulously regulated process essential for both normal development and pathological conditions, necessitates a comprehensive understanding of the endothelial mechanisms governing its Show more
Angiogenesis, a meticulously regulated process essential for both normal development and pathological conditions, necessitates a comprehensive understanding of the endothelial mechanisms governing its progression. Leveraging the zebrafish model and NgAgo knockdown system to identify target genes influencing angiogenesis, our study highlights the significant role of gastric inhibitory polypeptide (GIP) and its receptor (GIPR) in this process. While GIP has been extensively studied for its insulinotropic and glucagonotropic effects, its role in angiogenesis remains unexplored. This study demonstrated that GIPR knockdown induced developmental delays, morphological abnormalities, and pronounced angiogenic impairments in zebrafish embryos. Conversely, exogenous D-Ala2-GIP administration enhanced blood vessel formation in the yolk sac membrane of chick embryos. Consistent with these findings, D-Ala2-GIP treatment promoted microvessel formation in the tube formation assays and rat aortic ring models. Further investigation revealed that D-Ala2-GIP facilitated human umbilical vein endothelial cell (HUVEC) migration, a key step in angiogenesis, through the cyclic adenosine monophosphate (cAMP)-mediated activation of the Epac/Rap1/Cdc42 signaling pathway. This study provides novel insights into the angiogenic functions of GIP and its potential implications for cardiovascular biology. Show less
no PDF DOI: 10.1016/j.cellsig.2025.111615
GIPR

MicroRNA-6084 orchestrates angiogenesis and liver metastasis in colorectal cancer via extracellular vesicles.

Yang Zhang, Xuyang Yang, Su Zhang +10 more · 2025 · JCI insight · added 2026-04-24
The prognosis for colorectal cancer (CRC) patients with liver metastasis remains poor, and the molecular mechanisms driving CRC liver metastasis are not fully understood. Tumor-derived hypoxia-induced Show more
The prognosis for colorectal cancer (CRC) patients with liver metastasis remains poor, and the molecular mechanisms driving CRC liver metastasis are not fully understood. Tumor-derived hypoxia-induced extracellular vesicles have emerged as key players in inducing angiogenesis by transferring noncoding RNAs. However, the specific role of CRC-derived hypoxic extracellular vesicles (H-EVs) in regulating premetastatic microenvironment (PMN) formation by inducing angiogenesis remains unclear. Our study demonstrates that H-EVs induce angiogenesis and liver metastasis. Through microRNA microarray analysis, we identified a reduction in miR-6084 levels within H-EVs. We found that miR-6084 inhibited angiogenesis by being transferred to endothelial cells via EVs. In endothelial cells, miR-6084 directly targeted angiopoietin like 4 (ANGPTL4) mRNA, thereby suppressing angiogenesis through the ANGPTL4-mediated JAK2/STAT3 pathway. Furthermore, we uncovered that specificity protein 1 (SP1) acted as a transcription factor regulating miR-6084 transcription, while hypoxia-inducible factor 1A (HIF1A) decreased miR-6084 expression by promoting SP1 protein dephosphorylation and facilitating ubiquitin-proteasome degradation in SW620 cells. In clinical samples, we observed low expression of miR-6084 in plasma-derived EVs from CRC patients with liver metastasis. In summary, our findings suggest that CRC-derived H-EVs promote angiogenesis and liver metastasis through the HIF1A/SP1/miR-6084/ANGPTL4 axis. Additionally, miR-6084 holds promise as a diagnostic and prognostic biomarker for CRC liver metastasis. Show less
📄 PDF DOI: 10.1172/jci.insight.189503
ANGPTL4

E3 ligase HERC5-catalyzed UGDH isgylation promotes SNAI1-mediated tumor metastasis and cisplatin resistance in oral squamous cell carcinoma.

Xu Zhang, Fayu Liu, Qigen Fang +2 more · 2025 · Biology direct · BioMed Central · added 2026-04-24
Oral squamous cell carcinoma (OSCC) is one of the leading causes of cancer-related mortality worldwide due to its high aggressive potential and drug resistance. Previous studies have revealed an impor Show more
Oral squamous cell carcinoma (OSCC) is one of the leading causes of cancer-related mortality worldwide due to its high aggressive potential and drug resistance. Previous studies have revealed an important function of HECT And RLD Domain Containing E3 Ubiquitin Protein Ligase 5 (HERC5) in cancer. Six GEO gene microarrays identified HERC5 as a significant upregulated gene in OSCC tissues or cells (log2 Fold change > 1 and adj.p < 0.05). This study aimed to explore the role and underlying mechanisms of HERC5 in OSCC development. High HERC5 expression in OSCC tissues was confirmed by our hospital validation cohort and positively correlated with primary tumor stages. Subsequent functional studies demonstrated that knockdown of HERC5 inhibited the migratory and invasive capabilities with decrease of Vimentin and increase of E-cadherin in OSCC cells. In cisplatin treatment, cell survival rates were significantly reduced in HERC5-silencing OSCC cells, accompanied by the increase in cytotoxicity, DNA damage and apoptosis. OSCC cell-derived tumor xenograft displayed that HERC5 depletion inhibited pulmonary metastasis as well as restored the cisplatin-induced tumor burden. In line with this, overexpression of HERC5 yielded the opposite alterations both in vivo and in vitro. Mechanistically, UDP-glucose 6-dehydrogenase (UGDH) was identified as a HERC5-binding protein. Cysteine residue at position 994 in the HECT domain of HERC5 catalyzed the conjugation of ubiquitin-like protein Interferon-induced 15 kDa protein (ISG15) to UGDH (ISGylation of UGDH) and facilitated its phosphorylation, therefore enhancing SNAI1 mRNA stability. SNAI1 depletion inhibited HERC5 overexpression-triggered invasion and cisplatin resistance of OSCC cells. Our study indicates that HERC5 may be a promising therapeutic target for OSCC. Show less
no PDF DOI: 10.1186/s13062-025-00622-1
SNAI1

Significance of APOB/APOA1 Ratio in the Prediction of Calcific Aortic Valve Disease.

Yuxing Wang, Ming Yu, Song Yang +8 more · 2025 · Cardiovascular therapeutics · added 2026-04-24
📄 PDF DOI: 10.1155/cdr/5528174
APOB

COVID-19 infection and longevity: an observational and mendelian randomization study.

Shizheng Qiu, Jianhua Liu, Jiahe Guo +3 more · 2025 · Journal of translational medicine · BioMed Central · added 2026-04-24
Studies have indicated that COVID-19 infection may accelerate the aging process in organisms. However, it remains unknown whether contracting COVID-19 affects life expectancy. Furthermore, the underly Show more
Studies have indicated that COVID-19 infection may accelerate the aging process in organisms. However, it remains unknown whether contracting COVID-19 affects life expectancy. Furthermore, the underlying biological mechanisms behind these findings are still unclear. We conducted a prospective cohort study on 56,504 participants of European ancestry from the UK Biobank who reported the time and number of COVID-19 infection between January 2020 and September 2023. The parental average longevity was used as a proxy for their own longevity. Linear regression was used to assess the relationship between COVID-19 infection and longevity. Furthermore, we investigated the shared genetic basis between COVID-19 and longevity using large-scale genome-wide association studies (GWAS) for COVID-19 (122,616 cases and 2,475,240 controls) and longevity (3,484 cases and 25,483 controls). Mendelian randomization (MR) and mediation analysis were utilized to assess causal relationships and potential mediators between COVID-19 susceptibility and longevity. Shared genetic loci between the two phenotypes were identified using conjunctional false discovery rate (conjFDR) statistical frameworks. After controlling for relevant covariates, COVID-19 infection might not be significantly correlated with longevity. In all MR methods, generalized summary-data-based Mendelian randomization (GSMR) analysis revealed a significant decrease in longevity due to severe COVID-19 infection (OR = 0.91, 95%CI: 0.84-0.98, P = 0.015). Mediation analysis identified stroke and myocardial infarction as potential mediators between COVID-19 susceptibility and reduced longevity. At conjFDR < 0.05, we identified rs62062323 (KANSL1) and rs9530111 (PIBF1) as shared loci between COVID-19 and longevity. Together, our findings provided preliminary evidence for the shared genetic basics between COVID-19 and aging. This discovery may have implications for personalized medicine and preventive strategies, helping identify individuals who may be more vulnerable to severe outcomes from COVID-19 due to their genetic makeup. Show less
📄 PDF DOI: 10.1186/s12967-024-05932-y
KANSL1

Systematic Exploration of Potential Druggable Genes for Ischemic Stroke Employing Genome-Wide Mendelian Randomization Analysis.

Peng Zhang, Yulu He, Qing Zhen +1 more · 2025 · Brain and behavior · Wiley · added 2026-04-24
Ischemic stroke (IS) treatment remains a significant challenge. This study aimed to identify potential druggable genes for IS using a systematic druggable genome-wide Mendelian Randomization (MR) anal Show more
Ischemic stroke (IS) treatment remains a significant challenge. This study aimed to identify potential druggable genes for IS using a systematic druggable genome-wide Mendelian Randomization (MR) analysis. Two-sample MR analysis was conducted to identify the causal association between potential druggable genes and IS. This involved integrating data from the druggable genome, expression quantitative trait loci (eQTL), protein quantitative trait loci (pQTL), and genome-wide association study summary data of IS. Sensitivity and Bayesian colocalization analyses were used to validate the causal relationships. In addition, phenome-wide MR analysis was used to evaluate the side effects or other indications of the identified druggable genes, and their functions were explored using the Metascape database. Our MR analysis identified 16 potential druggable genes significantly associated with IS, three of which were significant in the two QTL datasets. Colocalization analysis revealed six druggable genes (two in the blood eQTL [CALCRL, KCNJ11], two in the brain eQTL [NEK3, THSD1], one in the blood pQTL [MMP12], and one in the brain pQTL [HSD17B12]) had a PP.H4 greater than 0.75. Phenome-wide MR analysis indicated that CALCRL is correlated with benign breast neoplasms, and HSD17B12 is associated with essential hypertension and hypertension. This study identified six potential druggable genes (CALCRL, KCNJ11, NEK3, THSD1, MMP12, and HSD17B12) associated with IS risk. Further research is required to explore the specific roles of these druggable genes in the onset and progression of IS. Show less
📄 PDF DOI: 10.1002/brb3.70857
HSD17B12

Identifying Key Epigenetic Modification-Related Genes for Cervical Squamous Cell Carcinoma and Endocervical Adenocarcinoma and Cellular Validation.

Huizhen Zhang, Junjie Li, Heng Xu +3 more · 2025 · Current gene therapy · Bentham Science · added 2026-04-24
Cervical Squamous Cell Carcinoma and Endocervical Adenocarcinoma (CESC) is a highly prevalent female malignancy. As the epigenomic characteristics of immune cells and cancer cells can serve as predict Show more
Cervical Squamous Cell Carcinoma and Endocervical Adenocarcinoma (CESC) is a highly prevalent female malignancy. As the epigenomic characteristics of immune cells and cancer cells can serve as predictive indicators for the response to cancer immunotherapy, analysis of epigenetically modified genes (EpiGenes) could contribute to CESC treatment. The ssGSEA algorithm was employed to compute EpiGenes scores. Core genes that exhibited significant module association and a close correlation with EpiGenes scores were identified via the WGCNA package. Univariate Cox proportional hazards regression was performed on the core genes using the survival package, followed by gene set reduction via LASSO Cox regression. Ultimately, key genes were determined through multivariate Cox regression to establish a RiskScore model. Further, the optimal risk cutoff was determined using the survminer package to stratify CESC patients into high- and low-risk subgroups. For enrichment analysis, clusterProfiler and GSEA were utilized. Immune infiltration across risk groups was evaluated via ssGSEA, the MCPcounter algorithm, and the ESTIMATE algorithm. TIDE was employed to compare immunotherapeutic responses between the risk groups, while the pRRophetic software was utilized to predict patients' chemotherapeutic drug sensitivity. The biomarkers identified were validated by performing in vitro experiments. CEP78, DOCK7, DPY19L4, and POM121 were identified by computational analyses as the key genes for CESC and further validated through in vitro experiments. Pathway enrichment analysis revealed predominant enrichment in immune-related pathways in the high-risk group, whereas the low-risk group was more enriched in energy and metabolic pathways. A significant negative correlation was observed between CD8+ T cell abundance and RiskScore, with higher ESTIMATEScores and StromalScores in high-risk patients. Notably, the high-risk group also demonstrated lower potential sensitivity to immunotherapy but more active responsiveness to a broader spectrum of chemotherapeutic agents. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis revealed that module genes are significantly enriched in cell cycle regulatory pathways, and these genes, in conjunction with Human Papillomavirus (HPV) infection-induced cell cycle dysregulation, jointly participate in CESC pathogenesis, providing a mechanistic basis for understanding the disease. This study provided novel theoretical evidence for immunotherapy and chemotherapy selection in the management of CESC. Show less
no PDF DOI: 10.2174/0115665232432474251103064112
DOCK7

Potential of CETP inhibition in treating dyslipidemia in systemic lupus erythematosus: Novel and comprehensive evidence from clinical studies and Mendelian randomization.

Yihong Gan, Yilin Zhang, Jingqun Liu +10 more · 2025 · International immunopharmacology · Elsevier · added 2026-04-24
Cardiovascular diseases from abnormal lipid metabolism significantly increase mortality in systemic lupus erythematosus (SLE). The causal link between dyslipidemia and SLE is unclear. Lipid metabolism Show more
Cardiovascular diseases from abnormal lipid metabolism significantly increase mortality in systemic lupus erythematosus (SLE). The causal link between dyslipidemia and SLE is unclear. Lipid metabolism in patients with SLE was evaluated based on clinical data from 511 patients with SLE and 706 healthy individuals. Bidirectional Mendelian randomization (MR) was employed to assess causal links between 179 plasma lipid metabolites, lipid-lowering drug targets, and SLE risk. Genetic instruments from GWAS and eQTL data were used to evaluate CETP and APOA4 effects. Peripheral blood CETP and apolipoprotein levels in SLE patients were validated via ELISA. SLE patients exhibited reduced HDL-C (P < 0.0001), APOA1 (P < 0.0001), and APOA4 (P < 0.0001), alongside elevated triglycerides (TG, P < 0.0001), APOC3, APOD, and APOF. MR identified three lipid metabolites-PC(18:2₂₀:4), TG(56:6), and TG(58:7)-as causal factors for SLE (P < 2.79E-5). CETP inhibition significantly reduced SLE risk via HDL-C modulation (OR = 0.72, P = 3.38E-08) and influenced LDL-C, TG, and apolipoproteins. Clinical validation confirmed elevated CETP and reduced APOA4 in SLE, correlating with disease activity. APOA4 activation showed protective effects, while PCSK9 inhibition lacked relevance. Bidirectional Mendelian randomization analyses confirmed dyslipidemia as a causal antecedent to SLE, with no evidence of reverse causation. A variety of MR analyses and clinical validation indicated that targeting HDL-C regulation offers significant advantages for managing dyslipidemia in patients with SLE, with CETP identified as the optimal pharmacological target. Show less
no PDF DOI: 10.1016/j.intimp.2025.114736
APOA4