👤 Yi-Ming Liu

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3182
Articles
1983
Name variants
Also published as: A Liu, Ai Liu, Ai-Guo Liu, Aidong Liu, Aiguo Liu, Aihua Liu, Aijun Liu, Ailing Liu, Aimin Liu, Allen P Liu, Aman Liu, An Liu, An-Qi Liu, Ang-Jun Liu, Anjing Liu, Anjun Liu, Ankang Liu, Anling Liu, Anmin Liu, Annuo Liu, Anshu Liu, Ao Liu, Aoxing Liu, B Liu, Baihui Liu, Baixue Liu, Baiyan Liu, Ban Liu, Bang Liu, Bang-Quan Liu, Bao Liu, Bao-Cheng Liu, Baogang Liu, Baohui Liu, Baolan Liu, Baoli Liu, Baoning Liu, Baoxin Liu, Baoyi Liu, Bei Liu, Beibei Liu, Ben Liu, Bi-Cheng Liu, Bi-Feng Liu, Bihao Liu, Bilin Liu, Bin Liu, Bing Liu, Bing-Wen Liu, Bingcheng Liu, Bingjie Liu, Bingwen Liu, Bingxiao Liu, Bingya Liu, Bingyu Liu, Binjie Liu, Bo Liu, Bo-Gong Liu, Bo-Han Liu, Boao Liu, Bolin Liu, Boling Liu, Boqun Liu, Bowen Liu, Boxiang Liu, Boxin Liu, Boya Liu, Boyang Liu, Brian Y Liu, C Liu, C M Liu, C Q Liu, C-T Liu, C-Y Liu, Caihong Liu, Cailing Liu, Caiyan Liu, Can Liu, Can-Zhao Liu, Catherine H Liu, Chan Liu, Chang Liu, Chang-Bin Liu, Chang-Hai Liu, Chang-Ming Liu, Chang-Pan Liu, Chang-Peng Liu, Changbin Liu, Changjiang Liu, Changliang Liu, Changming Liu, Changqing Liu, Changtie Liu, Changya Liu, Changyun Liu, Chao Liu, Chao-Ming Liu, Chaohong Liu, Chaoqi Liu, Chaoyi Liu, Chelsea Liu, Chen Liu, Chenchen Liu, Chendong Liu, Cheng Liu, Cheng-Li Liu, Cheng-Wu Liu, Cheng-Yong Liu, Cheng-Yun Liu, Chengbo Liu, Chenge Liu, Chengguo Liu, Chenghui Liu, Chengkun Liu, Chenglong Liu, Chengxiang Liu, Chengyao Liu, Chengyun Liu, Chenmiao Liu, Chenming Liu, Chenshu Liu, Chenxing Liu, Chenxu Liu, Chenxuan Liu, Chi Liu, Chia-Chen Liu, Chia-Hung Liu, Chia-Jen Liu, Chia-Yang Liu, Chia-Yu Liu, Chiang Liu, Chin-Chih Liu, Chin-Ching Liu, Chin-San Liu, Ching-Hsuan Liu, Ching-Ti Liu, Chong Liu, Christine S Liu, ChuHao Liu, Chuan Liu, Chuanfeng Liu, Chuanxin Liu, Chuanyang Liu, Chun Liu, Chun-Chi Liu, Chun-Feng Liu, Chun-Lei Liu, Chun-Ming Liu, Chun-Xiao Liu, Chun-Yu Liu, Chunchi Liu, Chundong Liu, Chunfeng Liu, Chung-Cheng Liu, Chung-Ji Liu, Chunhua Liu, Chunlei Liu, Chunliang Liu, Chunling Liu, Chunming Liu, Chunpeng Liu, Chunping Liu, Chunsheng Liu, Chunwei Liu, Chunxiao Liu, Chunyan Liu, Chunying Liu, Chunyu Liu, Cici Liu, Clarissa M Liu, Cong Cong Liu, Cong Liu, Congcong Liu, Cui Liu, Cui-Cui Liu, Cuicui Liu, Cuijie Liu, Cuilan Liu, Cun Liu, Cun-Fei Liu, D Liu, Da Liu, Da-Ren Liu, Daiyun Liu, Dajiang J Liu, Dan Liu, Dan-Ning Liu, Dandan Liu, Danhui Liu, Danping Liu, Dantong Liu, Danyang Liu, Danyong Liu, Daoshen Liu, David Liu, David R Liu, Dawei Liu, Daxu Liu, Dayong Liu, Dazhi Liu, De-Pei Liu, De-Shun Liu, Dechao Liu, Dehui Liu, Deliang Liu, Deng-Xiang Liu, Depei Liu, Deping Liu, Derek Liu, Deruo Liu, Desheng Liu, Dewu Liu, Dexi Liu, Deyao Liu, Deying Liu, Dezhen Liu, Di Liu, Didi Liu, Ding-Ming Liu, Dingding Liu, Dinglu Liu, Dingxiang Liu, Dong Liu, Dong-Yun Liu, Dongang Liu, Dongbo Liu, Dongfang Liu, Donghui Liu, Dongjuan Liu, Dongliang Liu, Dongmei Liu, Dongming Liu, Dongping Liu, Dongxian Liu, Dongxue Liu, Dongyan Liu, Dongyang Liu, Dongyao Liu, Dongzhou Liu, Dudu Liu, Dunjiang Liu, Edison Tak-Bun Liu, En-Qi Liu, Enbin Liu, Enlong Liu, Enqi Liu, Erdong Liu, Erfeng Liu, Erxiong Liu, F Liu, F Z Liu, Fan Liu, Fan-Jie Liu, Fang Liu, Fang-Zhou Liu, Fangli Liu, Fangmei Liu, Fangping Liu, Fangqi Liu, Fangzhou Liu, Fani Liu, Fayu Liu, Fei Liu, Feifan Liu, Feilong Liu, Feiyan Liu, Feiyang Liu, Feiye Liu, Fen Liu, Fendou Liu, Feng Liu, Feng-Ying Liu, Fengbin Liu, Fengchao Liu, Fengen Liu, Fengguo Liu, Fengjiao Liu, Fengjie Liu, Fengjuan Liu, Fengqiong Liu, Fengsong Liu, Fonda Liu, Foqiu Liu, Fu-Jun Liu, Fu-Tong Liu, Fubao Liu, Fuhao Liu, Fuhong Liu, Fujun Liu, Gan Liu, Gang Liu, Gangli Liu, Ganqiang Liu, Gaohua Liu, Ge Liu, Ge-Li Liu, Gen Sheng Liu, Geng Liu, Geng-Hao Liu, Geoffrey Liu, George E Liu, George Liu, Geroge Liu, Gexiu Liu, Gongguan Liu, Guang Liu, Guangbin Liu, Guangfan Liu, Guanghao Liu, Guangliang Liu, Guangqin Liu, Guangwei Liu, Guangxu Liu, Guannan Liu, Guantong Liu, Gui Yao Liu, Gui-Fen Liu, Gui-Jing Liu, Gui-Rong Liu, Guibo Liu, Guidong Liu, Guihong Liu, Guiju Liu, Guili Liu, Guiqiong Liu, Guiquan Liu, Guisheng Liu, Guiyou Liu, Guiyuan Liu, Guning Liu, Guo-Liang Liu, Guochang Liu, Guodong Liu, Guohao Liu, Guojun Liu, Guoke Liu, Guoliang Liu, Guopin Liu, Guoqiang Liu, Guoqing Liu, Guoquan Liu, Guowen Liu, Guoyong Liu, H Liu, Hai Feng Liu, Hai-Jing Liu, Hai-Xia Liu, Hai-Yan Liu, Haibin Liu, Haichao Liu, Haifei Liu, Haifeng Liu, Hailan Liu, Hailin Liu, Hailing Liu, Haitao Liu, Haiyan Liu, Haiyang Liu, Haiying Liu, Haizhao Liu, Han Liu, Han-Fu Liu, Han-Qi Liu, Hancong Liu, Hang Liu, Hanhan Liu, Hanjiao Liu, Hanjie Liu, Hanmin Liu, Hanqing Liu, Hanxiang Liu, Hanyuan Liu, Hao Liu, Haobin Liu, Haodong Liu, Haogang Liu, Haojie Liu, Haokun Liu, Haoling Liu, Haowei Liu, Haowen Liu, Haoyue Liu, He-Kun Liu, Hehe Liu, Hekun Liu, Heliang Liu, Heng Liu, Hengan Liu, Hengru Liu, Hengtong Liu, Heyi Liu, Hong Juan Liu, Hong Liu, Hong Wei Liu, Hong-Bin Liu, Hong-Li Liu, Hong-Liang Liu, Hong-Tao Liu, Hong-Xiang Liu, Hong-Ying Liu, Hongbin Liu, Hongbing Liu, Hongfa Liu, Honghan Liu, Honghe Liu, Hongjian Liu, Hongjie Liu, Hongjun Liu, Hongli Liu, Hongliang Liu, Hongmei Liu, Hongqun Liu, Hongtao Liu, Hongwei Liu, Hongxiang Liu, Hongxing Liu, Hongyan Liu, Hongyang Liu, Hongyao Liu, Hongyu Liu, Hongyuan Liu, Houbao Liu, Hsiao-Ching Liu, Hsiao-Sheng Liu, Hsiaowei Liu, Hsu-Hsiang Liu, Hu Liu, Hua Liu, Hua-Cheng Liu, Hua-Ge Liu, Huadong Liu, Huaizheng Liu, Huan Liu, Huan-Yu Liu, Huanhuan Liu, Huanliang Liu, Huanyi Liu, Huatao Liu, Huawei Liu, Huayang Liu, Huazhen Liu, Hui Liu, Hui-Chao Liu, Hui-Fang Liu, Hui-Guo Liu, Hui-Hui Liu, Hui-Xin Liu, Hui-Ying Liu, Huibin Liu, Huidi Liu, Huihua Liu, Huihui Liu, Huijuan Liu, Huijun Liu, Huikun Liu, Huiling Liu, Huimao Liu, Huimin Liu, Huiming Liu, Huina Liu, Huiping Liu, Huiqing Liu, Huisheng Liu, Huiying Liu, Huiyu Liu, Hulin Liu, J Liu, J R Liu, J W Liu, J X Liu, J Z Liu, James K C Liu, Jamie Liu, Jay Liu, Ji Liu, Ji-Kai Liu, Ji-Long Liu, Ji-Xing Liu, Ji-Xuan Liu, Ji-Yun Liu, Jia Liu, Jia-Cheng Liu, Jia-Jun Liu, Jia-Qian Liu, Jia-Yao Liu, JiaXi Liu, Jiabin Liu, Jiachen Liu, Jiahao Liu, Jiahua Liu, Jiahui Liu, Jiajie Liu, Jiajuan Liu, Jiakun Liu, Jiali Liu, Jialin Liu, Jiamin Liu, Jiaming Liu, Jian Liu, Jian-Jun Liu, Jian-Kun Liu, Jian-hong Liu, Jian-shu Liu, Jianan Liu, Jianbin Liu, Jianbo Liu, Jiandong Liu, Jianfang Liu, Jianfeng Liu, Jiang Liu, Jiangang Liu, Jiangbin Liu, Jianghong Liu, Jianghua Liu, Jiangjiang Liu, Jiangjin Liu, Jiangling Liu, Jiangxin Liu, Jiangyan Liu, Jianhua Liu, Jianhui Liu, Jiani Liu, Jianing Liu, Jianjiang Liu, Jianjun Liu, Jiankang Liu, Jiankun Liu, Jianlei Liu, Jianmei Liu, Jianmin Liu, Jiannan Liu, Jianping Liu, Jiantao Liu, Jianwei Liu, Jianxi Liu, Jianxin Liu, Jianyong Liu, Jianyu Liu, Jianyun Liu, Jiao Liu, Jiaojiao Liu, Jiaoyang Liu, Jiaqi Liu, Jiaqing Liu, Jiawen Liu, Jiaxian Liu, Jiaxiang Liu, Jiaxin Liu, Jiayan Liu, Jiayi Liu, Jiayin Liu, Jiaying Liu, Jiayu Liu, Jiayun Liu, Jiazhe Liu, Jiazheng Liu, Jiazhuo Liu, Jidan Liu, Jie Liu, Jie-Qing Liu, Jierong Liu, Jiewei Liu, Jiewen Liu, Jieying Liu, Jieyu Liu, Jihe Liu, Jiheng Liu, Jin Liu, Jin-Juan Liu, Jin-Qing Liu, Jinbao Liu, Jinbo Liu, Jincheng Liu, Jindi Liu, Jinfeng Liu, Jing Liu, Jing Min Liu, Jing-Crystal Liu, Jing-Hua Liu, Jing-Ying Liu, Jing-Yu Liu, Jingbo Liu, Jingchong Liu, Jingfang Liu, Jingfeng Liu, Jingfu Liu, Jinghui Liu, Jingjie Liu, Jingjing Liu, Jingmeng Liu, Jingmin Liu, Jingqi Liu, Jingquan Liu, Jingqun Liu, Jingsheng Liu, Jingwei Liu, Jingwen Liu, Jingxing Liu, Jingyi Liu, Jingying Liu, Jingyun Liu, Jingzhong Liu, Jinjie Liu, Jinlian Liu, Jinlong Liu, Jinman Liu, Jinpei Liu, Jinpeng Liu, Jinping Liu, Jinqin Liu, Jinrong Liu, Jinsheng Liu, Jinsong Liu, Jinsuo Liu, Jinxiang Liu, Jinxin Liu, Jinxing Liu, Jinyue Liu, Jinze Liu, Jinzhao Liu, Jinzhi Liu, Jiong Liu, Jishan Liu, Jitao Liu, Jiwei Liu, Jixin Liu, Jonathan Liu, Joyce F Liu, Joyce Liu, Ju Liu, Ju-Fang Liu, Juan Liu, Juanjuan Liu, Juanxi Liu, Jue Liu, Jui-Tung Liu, Jun Liu, Jun O Liu, Jun Ting Liu, Jun Yi Liu, Jun-Jen Liu, Jun-Yan Liu, Jun-Yi Liu, Junbao Liu, Junchao Liu, Junfen Liu, Junhui Liu, Junjiang Liu, Junjie Liu, Junjin Liu, Junjun Liu, Junlin Liu, Junling Liu, Junnian Liu, Junpeng Liu, Junqi Liu, Junrong Liu, Juntao Liu, Juntian Liu, Junwen Liu, Junwu Liu, Junxi Liu, Junyan Liu, Junye Liu, Junying Liu, Junyu Liu, Juyao Liu, Kai Liu, Kai-Zheng Liu, Kaidong Liu, Kaijing Liu, Kaikun Liu, Kaiqi Liu, Kaisheng Liu, Kaitai Liu, Kaiwen Liu, Kang Liu, Kang-le Liu, Kangdong Liu, Kangwei Liu, Kathleen D Liu, Ke Liu, Ke-Tong Liu, Kechun Liu, Kehui Liu, Kejia Liu, Keng-Hau Liu, Keqiang Liu, Kexin Liu, Kiang Liu, Kuangyi Liu, Kun Liu, Kun-Cheng Liu, Kwei-Yan Liu, L L Liu, L Liu, L W Liu, Lan Liu, Lan-Xiang Liu, Lang Liu, Lanhao Liu, Le Liu, Lebin Liu, Lei Liu, Lele Liu, Leping Liu, Li Liu, Li-Fang Liu, Li-Min Liu, Li-Rong Liu, Li-Wen Liu, Li-Xuan Liu, Li-Ying Liu, Li-ping Liu, Lian Liu, Lianfei Liu, Liang Liu, Liang-Chen Liu, Liang-Feng Liu, Liangguo Liu, Liangji Liu, Liangjia Liu, Liangliang Liu, Liangyu Liu, Lianxin Liu, Lianyong Liu, Libin Liu, Lichao Liu, Lichun Liu, Lidong Liu, Liegang Liu, Lifang Liu, Ligang Liu, Lihua Liu, Lijuan Liu, Lijun Liu, Lili Liu, Liling Liu, Limin Liu, Liming Liu, Lin Liu, Lina Liu, Ling Liu, Ling-Yun Liu, Ling-Zhi Liu, Lingfei Liu, Lingjiao Liu, Lingjuan Liu, Linglong Liu, Lingyan Liu, Lining Liu, Linlin Liu, Linqing Liu, Linwen Liu, Liping Liu, Liqing Liu, Liqiong Liu, Liqun Liu, Lirong Liu, Liru Liu, Liu Liu, Liumei Liu, Liusheng Liu, Liwen Liu, Lixia Liu, Lixian Liu, Lixiao Liu, Liying Liu, Liyue Liu, Lizhen Liu, Long Liu, Longfei Liu, Longjian Liu, Longqian Liu, Longyang Liu, Longzhou Liu, Lu Liu, Luhong Liu, Lulu Liu, Luming Liu, Lunxu Liu, Luping Liu, Lushan Liu, Lv Liu, M L Liu, M Liu, Man Liu, Man-Ru Liu, Manjiao Liu, Manqi Liu, Manran Liu, Maolin Liu, Mei Liu, Mei-mei Liu, Meicen Liu, Meifang Liu, Meijiao Liu, Meijing Liu, Meijuan Liu, Meijun Liu, Meiling Liu, Meimei Liu, Meixin Liu, Meiyan Liu, Meng Han Liu, Meng Liu, Meng-Hui Liu, Meng-Meng Liu, Meng-Yue Liu, Mengduan Liu, Mengfan Liu, Mengfei Liu, Menggang Liu, Menghan Liu, Menghua Liu, Menghui Liu, Mengjia Liu, Mengjiao Liu, Mengke Liu, Menglin Liu, Mengling Liu, Mengmei Liu, Mengqi Liu, Mengqian Liu, Mengxi Liu, Mengxue Liu, Mengyang Liu, Mengying Liu, Mengyu Liu, Mengyuan Liu, Mengzhen Liu, Mi Liu, Mi-Hua Liu, Mi-Min Liu, Miao Liu, Miaoliang Liu, Min Liu, Minda Liu, Minetta C Liu, Ming Liu, Ming-Jiang Liu, Ming-Qi Liu, Mingcheng Liu, Mingchun Liu, Mingfan Liu, Minghui Liu, Mingjiang Liu, Mingjing Liu, Mingjun Liu, Mingli Liu, Mingming Liu, Mingna Liu, Mingqin Liu, Mingrui Liu, Mingsen Liu, Mingsong Liu, Mingxiao Liu, Mingxing Liu, Mingxu Liu, Mingyang Liu, Mingyao Liu, Mingying Liu, Mingyu Liu, Minhao Liu, Minxia Liu, Mo-Nan Liu, Modan Liu, Mouze Liu, Muqiu Liu, Musang Liu, N A Liu, N Liu, Na Liu, Na-Nv Liu, Na-Wei Liu, Nai-feng Liu, Naihua Liu, Naili Liu, Nan Liu, Nan-Song Liu, Nana Liu, Nannan Liu, Nanxi Liu, Ni Liu, Nian Liu, Ning Liu, Ning'ang Liu, Ningning Liu, Niya Liu, Ou Liu, Ouxuan Liu, P C Liu, Pan Liu, Panhong Liu, Panting Liu, Paul Liu, Pei Liu, Pei-Ning Liu, Peijian Liu, Peijie Liu, Peijun Liu, Peilong Liu, Peiqi Liu, Peiqing Liu, Peiwei Liu, Peixi Liu, Peiyao Liu, Peizhong Liu, Peng Liu, Pengcheng Liu, Pengfei Liu, Penghong Liu, Pengli Liu, Pengtao Liu, Pengyu Liu, Pengyuan Liu, Pentao Liu, Peter S Liu, Piaopiao Liu, Pinduo Liu, Ping Liu, Ping-Yen Liu, Pinghuai Liu, Pingping Liu, Pingsheng Liu, Q Liu, Qi Liu, Qi-Xian Liu, Qian Liu, Qian-Wen Liu, Qiang Liu, Qiang-Yuan Liu, Qiangyun Liu, Qianjin Liu, Qianqi Liu, Qianshuo Liu, Qianwei Liu, Qiao-Hong Liu, Qiaofeng Liu, Qiaoyan Liu, Qiaozhen Liu, Qiji Liu, Qiming Liu, Qin Liu, Qinfang Liu, Qing Liu, Qing-Huai Liu, Qing-Rong Liu, Qingbin Liu, Qingbo Liu, Qingguang Liu, Qingguo Liu, Qinghao Liu, Qinghong Liu, Qinghua Liu, Qinghuai Liu, Qinghuan Liu, Qinglei Liu, Qingping Liu, Qingqing Liu, Qingquan Liu, Qingsong Liu, Qingxia Liu, Qingxiang Liu, Qingyang Liu, Qingyou Liu, Qingyun Liu, Qingzhuo Liu, Qinqin Liu, Qiong Liu, Qiu-Ping Liu, Qiulei Liu, Qiuli Liu, Qiulu Liu, Qiushi Liu, Qiuxu Liu, Qiuyu Liu, Qiuyue Liu, Qiwei Liu, Qiyao Liu, Qiye Liu, Qizhan Liu, Quan Liu, Quan-Jun Liu, Quanxin Liu, Quanying Liu, Quanzhong Liu, Quentin Liu, Qun Liu, Qunlong Liu, Qunpeng Liu, R F Liu, R Liu, R Y Liu, Ran Liu, Rangru Liu, Ranran Liu, Ren Liu, Renling Liu, Ri Liu, Rong Liu, Rong-Zong Liu, Rongfei Liu, Ronghua Liu, Rongxia Liu, Rongxun Liu, Rui Liu, Rui-Jie Liu, Rui-Tian Liu, Rui-Xuan Liu, Ruichen Liu, Ruihua Liu, Ruijie Liu, Ruijuan Liu, Ruilong Liu, Ruiping Liu, Ruiqi Liu, Ruitong Liu, Ruixia Liu, Ruiyi Liu, Ruizao Liu, Runjia Liu, Runjie Liu, Runni Liu, Runping Liu, Ruochen Liu, Ruotian Liu, Ruowen Liu, Ruoyang Liu, Ruyi Liu, Ruyue Liu, S Liu, Saiji Liu, Sasa Liu, Sen Liu, Senchen Liu, Senqi Liu, Sha Liu, Shan Liu, Shan-Shan Liu, Shandong Liu, Shang-Feng Liu, Shang-Xin Liu, Shangjing Liu, Shangxin Liu, Shangyu Liu, Shangyuan Liu, Shangyun Liu, Shanhui Liu, Shanling Liu, Shanshan Liu, Shao-Bin Liu, Shao-Jun Liu, Shao-Yuan Liu, Shaobo Liu, Shaocheng Liu, Shaohua Liu, Shaojun Liu, Shaoqing Liu, Shaowei Liu, Shaoying Liu, Shaoyou Liu, Shaoyu Liu, Shaozhen Liu, Shasha Liu, Sheng Liu, Shengbin Liu, Shengjun Liu, Shengnan Liu, Shengyang Liu, Shengzhi Liu, Shengzhuo Liu, Shenhai Liu, Shenping Liu, Shi Liu, Shi-Lian Liu, Shi-Wei Liu, Shi-Yong Liu, Shi-guo Liu, ShiWei Liu, Shih-Ping Liu, Shijia Liu, Shijian Liu, Shijie Liu, Shijun Liu, Shikai Liu, Shikun Liu, Shilin Liu, Shing-Hwa Liu, Shiping Liu, Shiqian Liu, Shiquan Liu, Shiru Liu, Shixi Liu, Shiyan Liu, Shiyang Liu, Shiying Liu, Shiyu Liu, Shiyuan Liu, Shou-Sheng Liu, Shouguo Liu, Shoupei Liu, Shouxin Liu, Shouyang Liu, Shu Liu, Shu-Chen Liu, Shu-Jing Liu, Shu-Lin Liu, Shu-Qiang Liu, Shu-Qin Liu, Shuai Liu, Shuaishuai Liu, Shuang Liu, Shuangli Liu, Shuangzhu Liu, Shuhong Liu, Shuhua Liu, Shui-Bing Liu, Shujie Liu, Shujing Liu, Shujun Liu, Shulin Liu, Shuling Liu, Shumin Liu, Shun-Mei Liu, Shunfang Liu, Shuning Liu, Shunming Liu, Shuqian Liu, Shuqing Liu, Shuwen Liu, Shuxi Liu, Shuxian Liu, Shuya Liu, Shuyan Liu, Shuyu Liu, Si-Jin Liu, Si-Xu Liu, Si-Yan Liu, Si-jun Liu, Sicheng Liu, Sidan Liu, Side Liu, Sihao Liu, Sijing Liu, Sijun Liu, Silvia Liu, Simin Liu, Sipu Liu, Siqi Liu, Siqin Liu, Siru Liu, Sirui Liu, Sisi Liu, Sitian Liu, Siwen Liu, Sixi Liu, Sixin Liu, Sixiu Liu, Sixu Liu, Siyao Liu, Siyi Liu, Siyu Liu, Siyuan Liu, Song Liu, Song-Fang Liu, Song-Mei Liu, Song-Ping Liu, Songfang Liu, Songhui Liu, Songqin Liu, Songsong Liu, Songyi Liu, Su Liu, Su-Yun Liu, Sudong Liu, Suhuan Liu, Sui-Feng Liu, Suling Liu, Suosi Liu, Sushuang Liu, Susu Liu, Szu-Heng Liu, T H Liu, T Liu, Ta-Chih Liu, Taihang Liu, Taixiang Liu, Tang Liu, Tao Liu, Taoli Liu, Taotao Liu, Te Liu, Teng Liu, Tengfei Liu, Tengli Liu, Teresa T Liu, Tian Liu, Tian Shu Liu, Tianhao Liu, Tianhu Liu, Tianjia Liu, Tianjiao Liu, Tianlai Liu, Tianlang Liu, Tianlong Liu, Tianqiang Liu, Tianrui Liu, Tianshu Liu, Tiantian Liu, Tianyao Liu, Tianyi Liu, Tianyu Liu, Tianze Liu, Tiemin Liu, Tina Liu, Ting Liu, Ting-Li Liu, Ting-Ting Liu, Ting-Yuan Liu, Tingjiao Liu, Tingting Liu, Tong Liu, Tonglin Liu, Tongtong Liu, Tongyan Liu, Tongyu Liu, Tongyun Liu, Tongzheng Liu, Tsang-Wu Liu, Tsung-Yun Liu, Vincent W S Liu, W Liu, W-Y Liu, Wan Liu, Wan-Chun Liu, Wan-Di Liu, Wan-Guo Liu, Wan-Ying Liu, Wang Liu, Wangrui Liu, Wanguo Liu, Wangyang Liu, Wanjun Liu, Wanli Liu, Wanlu Liu, Wanqi Liu, Wanqing Liu, Wanting Liu, Wei Liu, Wei-Chieh Liu, Wei-Hsuan Liu, Wei-Hua Liu, Weida Liu, Weifang Liu, Weifeng Liu, Weiguo Liu, Weihai Liu, Weihong Liu, Weijian Liu, Weijie Liu, Weijun Liu, Weilin Liu, Weimin Liu, Weiming Liu, Weina Liu, Weiqin Liu, Weiqing Liu, Weiren Liu, Weisheng Liu, Weishuo Liu, Weiwei Liu, Weiyang Liu, Wen Liu, Wen Yuan Liu, Wen-Chun Liu, Wen-Di Liu, Wen-Fang Liu, Wen-Jie Liu, Wen-Jing Liu, Wen-Qiang Liu, Wen-Tao Liu, Wen-ling Liu, Wenbang Liu, Wenbin Liu, Wenbo Liu, Wenchao Liu, Wenen Liu, Wenfeng Liu, Wenhan Liu, Wenhao Liu, Wenhua Liu, Wenjie Liu, Wenjing Liu, Wenlang Liu, Wenli Liu, Wenling Liu, Wenlong Liu, Wenna Liu, Wenping Liu, Wenqi Liu, Wenrui Liu, Wensheng Liu, Wentao Liu, Wenwu Liu, Wenxiang Liu, Wenxuan Liu, Wenya Liu, Wenyan Liu, Wenyi Liu, Wenzhong Liu, Wu Liu, Wuping Liu, Wuyang Liu, X C Liu, X Liu, X P Liu, X-D Liu, Xi Liu, Xi-Yu Liu, Xia Liu, Xia-Meng Liu, Xialin Liu, Xian Liu, Xianbao Liu, Xianchen Liu, Xianda Liu, Xiang Liu, Xiang-Qian Liu, Xiang-Yu Liu, Xiangchen Liu, Xiangfei Liu, Xianglan Liu, Xiangli Liu, Xiangliang Liu, Xianglu Liu, Xiangning Liu, Xiangping Liu, Xiangsheng Liu, Xiangtao Liu, Xiangting Liu, Xiangxiang Liu, Xiangxuan Liu, Xiangyong Liu, Xiangyu Liu, Xiangyun Liu, Xianli Liu, Xianling Liu, Xiansheng Liu, Xianyang Liu, Xiao Dong Liu, Xiao Liu, Xiao Yan Liu, Xiao-Cheng Liu, Xiao-Dan Liu, Xiao-Gang Liu, Xiao-Guang Liu, Xiao-Huan Liu, Xiao-Jiao Liu, Xiao-Li Liu, Xiao-Ling Liu, Xiao-Ning Liu, Xiao-Qiu Liu, Xiao-Qun Liu, Xiao-Rong Liu, Xiao-Song Liu, Xiao-Xiao Liu, Xiao-lan Liu, Xiaoan Liu, Xiaobai Liu, Xiaobei Liu, Xiaobing Liu, Xiaocen Liu, Xiaochuan Liu, Xiaocong Liu, Xiaodan Liu, Xiaoding Liu, Xiaodong Liu, Xiaofan Liu, Xiaofang Liu, Xiaofei Liu, Xiaogang Liu, Xiaoguang Liu, Xiaoguang Margaret Liu, Xiaohan Liu, Xiaoheng Liu, Xiaohong Liu, Xiaohua Liu, Xiaohuan Liu, Xiaohui Liu, Xiaojie Liu, Xiaojing Liu, Xiaoju Liu, Xiaojun Liu, Xiaole Shirley Liu, Xiaolei Liu, Xiaoli Liu, Xiaolin Liu, Xiaoling Liu, Xiaoman Liu, Xiaomei Liu, Xiaomeng Liu, Xiaomin Liu, Xiaoming Liu, Xiaona Liu, Xiaonan Liu, Xiaopeng Liu, Xiaoping Liu, Xiaoqian Liu, Xiaoqiang Liu, Xiaoqin Liu, Xiaoqing Liu, Xiaoran Liu, Xiaosong Liu, Xiaotian Liu, Xiaoting Liu, Xiaowei Liu, Xiaoxi Liu, Xiaoxia Liu, Xiaoxiao Liu, Xiaoxu Liu, Xiaoxue Liu, Xiaoya Liu, Xiaoyan Liu, Xiaoyang Liu, Xiaoye Liu, Xiaoying Liu, Xiaoyong Liu, Xiaoyu Liu, Xiawen Liu, Xibao Liu, Xibing Liu, Xie-hong Liu, Xiehe Liu, Xiguang Liu, Xijun Liu, Xili Liu, Xin Liu, Xin-Hua Liu, Xin-Yan Liu, Xinbo Liu, Xinchang Liu, Xing Liu, Xing-De Liu, Xing-Li Liu, Xing-Yang Liu, Xingbang Liu, Xingde Liu, Xinghua Liu, Xinghui Liu, Xingjing Liu, Xinglei Liu, Xingli Liu, Xinglong Liu, Xinguo Liu, Xingxiang Liu, Xingyi Liu, Xingyu Liu, Xinhua Liu, Xinjun Liu, Xinlei Liu, Xinli Liu, Xinmei Liu, Xinmin Liu, Xinran Liu, Xinru Liu, Xinrui Liu, Xintong Liu, Xinxin Liu, Xinyao Liu, Xinyi Liu, Xinying Liu, Xinyong Liu, Xinyu Liu, Xinyue Liu, Xiong Liu, Xiqiang Liu, Xiru Liu, Xishan Liu, Xiu Liu, Xiufen Liu, Xiufeng Liu, Xiuheng Liu, Xiuling Liu, Xiumei Liu, Xiuqin Liu, Xiyong Liu, Xu Liu, Xu-Dong Liu, Xu-Hui Liu, Xuan Liu, Xuanlin Liu, Xuanyu Liu, Xuanzhu Liu, Xue Liu, Xue-Lian Liu, Xue-Min Liu, Xue-Qing Liu, Xue-Zheng Liu, Xuefang Liu, Xuejing Liu, Xuekui Liu, Xuelan Liu, Xueling Liu, Xuemei Liu, Xuemeng Liu, Xuemin Liu, Xueping Liu, Xueqin Liu, Xueqing Liu, Xueru Liu, Xuesen Liu, Xueshibojie Liu, Xuesong Liu, Xueting Liu, Xuewei Liu, Xuewen Liu, Xuexiu Liu, Xueying Liu, Xueyuan Liu, Xuezhen Liu, Xuezheng Liu, Xuezhi Liu, Xufeng Liu, Xuguang Liu, Xujie Liu, Xulin Liu, Xuming Liu, Xunhua Liu, Xunyue Liu, Xuxia Liu, Xuxu Liu, Xuyi Liu, Xuying Liu, Y H Liu, Y L Liu, Y Liu, Y Y Liu, Ya Liu, Ya-Jin Liu, Ya-Kun Liu, Ya-Wei Liu, Yadong Liu, Yafei Liu, Yajing Liu, Yajuan Liu, Yaling Liu, Yalu Liu, Yan Liu, Yan-Li Liu, Yanan Liu, Yanchao Liu, Yanchen Liu, Yandong Liu, Yanfei Liu, Yanfen Liu, Yanfeng Liu, Yang Liu, Yange Liu, Yangfan Liu, Yangfan P Liu, Yangjun Liu, Yangkai Liu, Yangruiyu Liu, Yangyang Liu, Yanhong Liu, Yanhua Liu, Yanhui Liu, Yanjie Liu, Yanju Liu, Yanjun Liu, Yankuo Liu, Yanli Liu, Yanliang Liu, Yanling Liu, Yanman Liu, Yanmin Liu, Yanping Liu, Yanqing Liu, Yanqiu Liu, Yanquan Liu, Yanru Liu, Yansheng Liu, Yansong Liu, Yanting Liu, Yanwu Liu, Yanxiao Liu, Yanyan Liu, Yanyao Liu, Yanying Liu, Yanyun Liu, Yao Liu, Yao-Hui Liu, Yaobo Liu, Yaoquan Liu, Yaou Liu, Yaowen Liu, Yaoyao Liu, Yaozhong Liu, Yaping Liu, Yaqiong Liu, Yarong Liu, Yaru Liu, Yating Liu, Yaxin Liu, Ye Liu, Ye-Dan Liu, Yehai Liu, Yen-Chen Liu, Yen-Chun Liu, Yen-Nien Liu, Yeqing Liu, Yi Liu, Yi-Chang Liu, Yi-Chien Liu, Yi-Han Liu, Yi-Hung Liu, Yi-Jia Liu, Yi-Ling Liu, Yi-Meng Liu, Yi-Yun Liu, Yi-Zhang Liu, YiRan Liu, Yibin Liu, Yibing Liu, Yicun Liu, Yidan Liu, Yidong Liu, Yifan Liu, Yifu Liu, Yihao Liu, Yiheng Liu, Yihui Liu, Yijing Liu, Yilei Liu, Yili Liu, Yilin Liu, Yimei Liu, Yiming Liu, Yin Liu, Yin-Ping Liu, Yinchu Liu, Yinfang Liu, Ying Liu, Ying Poi Liu, Yingchun Liu, Yinghua Liu, Yinghuan Liu, Yinghui Liu, Yingjun Liu, Yingli Liu, Yingwei Liu, Yingxia Liu, Yingyan Liu, Yingyi Liu, Yingying Liu, Yingzi Liu, Yinhe Liu, Yinhui Liu, Yining Liu, Yinjiang Liu, Yinping Liu, Yinuo Liu, Yiping Liu, Yiqing Liu, Yitian Liu, Yiting Liu, Yitong Liu, Yiwei Liu, Yiwen Liu, Yixiang Liu, Yixiao Liu, Yixuan Liu, Yiyang Liu, Yiyi Liu, Yiyuan Liu, Yiyun Liu, Yizhi Liu, Yizhuo Liu, Yong Liu, Yong Mei Liu, Yong-Chao Liu, Yong-Hong Liu, Yong-Jian Liu, Yong-Jun Liu, Yong-Tai Liu, Yong-da Liu, Yongchao Liu, Yonggang Liu, Yonggao Liu, Yonghong Liu, Yonghua Liu, Yongjian Liu, Yongjie Liu, Yongjun Liu, Yongli Liu, Yongmei Liu, Yongming Liu, Yongqiang Liu, Yongshuo Liu, Yongtai Liu, Yongtao Liu, Yongtong Liu, Yongxiao Liu, Yongyue Liu, You Liu, You-ping Liu, Youan Liu, Youbin Liu, Youdong Liu, Youhan Liu, Youlian Liu, Youwen Liu, Yu Liu, Yu Xuan Liu, Yu-Chen Liu, Yu-Ching Liu, Yu-Hui Liu, Yu-Li Liu, Yu-Lin Liu, Yu-Peng Liu, Yu-Wei Liu, Yu-Zhang Liu, YuHeng Liu, Yuan Liu, Yuan-Bo Liu, Yuan-Jie Liu, Yuan-Tao Liu, YuanHua Liu, Yuanchu Liu, Yuanfa Liu, Yuanhang Liu, Yuanhui Liu, Yuanjia Liu, Yuanjiao Liu, Yuanjun Liu, Yuanliang Liu, Yuantao Liu, Yuantong Liu, Yuanxiang Liu, Yuanxin Liu, Yuanxing Liu, Yuanying Liu, Yuanyuan Liu, Yubin Liu, Yuchen Liu, Yue Liu, Yuecheng Liu, Yuefang Liu, Yuehong Liu, Yueli Liu, Yueping Liu, Yuetong Liu, Yuexi Liu, Yuexin Liu, Yuexing Liu, Yueyang Liu, Yueyun Liu, Yufan Liu, Yufei Liu, Yufeng Liu, Yuhao Liu, Yuhe Liu, Yujia Liu, Yujiang Liu, Yujie Liu, Yujun Liu, Yulan Liu, Yuling Liu, Yulong Liu, Yumei Liu, Yumiao Liu, Yun Liu, Yun-Cai Liu, Yun-Qiang Liu, Yun-Ru Liu, Yun-Zi Liu, Yunfen Liu, Yunfeng Liu, Yuning Liu, Yunjie Liu, Yunlong Liu, Yunqi Liu, Yunqiang Liu, Yuntao Liu, Yunuan Liu, Yunuo Liu, Yunxia Liu, Yunyun Liu, Yuping Liu, Yupu Liu, Yuqi Liu, Yuqiang Liu, Yuqing Liu, Yurong Liu, Yuru Liu, Yusen Liu, Yutao Liu, Yutian Liu, Yuting Liu, Yutong Liu, Yuwei Liu, Yuxi Liu, Yuxia Liu, Yuxiang Liu, Yuxin Liu, Yuxuan Liu, Yuyan Liu, Yuyi Liu, Yuyu Liu, Yuyuan Liu, Yuzhen Liu, Yv-Xuan Liu, Z H Liu, Z Q Liu, Z Z Liu, Zaiqiang Liu, Zan Liu, Zaoqu Liu, Ze Liu, Zefeng Liu, Zekun Liu, Zeming Liu, Zengfu Liu, Zeyu Liu, Zezhou Liu, Zhangyu Liu, Zhangyuan Liu, Zhansheng Liu, Zhao Liu, Zhaoguo Liu, Zhaoli Liu, Zhaorui Liu, Zhaotian Liu, Zhaoxiang Liu, Zhaoxun Liu, Zhaoyang Liu, Zhe Liu, Zhekai Liu, Zheliang Liu, Zhen Liu, Zhen-Lin Liu, Zhendong Liu, Zhenfang Liu, Zhenfeng Liu, Zheng Liu, Zheng-Hong Liu, Zheng-Yu Liu, ZhengYi Liu, Zhengbing Liu, Zhengchuang Liu, Zhengdong Liu, Zhenghao Liu, Zhengkun Liu, Zhengtang Liu, Zhengting Liu, Zhenguo Liu, Zhengxia Liu, Zhengye Liu, Zhenhai Liu, Zhenhao Liu, Zhenhua Liu, Zhenjiang Liu, Zhenjiao Liu, Zhenjie Liu, Zhenkui Liu, Zhenlei Liu, Zhenmi Liu, Zhenming Liu, Zhenna Liu, Zhenqian Liu, Zhenqiu Liu, Zhenwei Liu, Zhenxing Liu, Zhenxiu Liu, Zhenzhen Liu, Zhenzhu Liu, Zhi Liu, Zhi Y Liu, Zhi-Fen Liu, Zhi-Guo Liu, Zhi-Jie Liu, Zhi-Kai Liu, Zhi-Ping Liu, Zhi-Ren Liu, Zhi-Wen Liu, Zhi-Ying Liu, Zhicheng Liu, Zhifang Liu, Zhigang Liu, Zhiguo Liu, Zhihan Liu, Zhihao Liu, Zhihong Liu, Zhihua Liu, Zhihui Liu, Zhijia Liu, Zhijie Liu, Zhikui Liu, Zhili Liu, Zhiming Liu, Zhipeng Liu, Zhiping Liu, Zhiqian Liu, Zhiqiang Liu, Zhiru Liu, Zhirui Liu, Zhishuo Liu, Zhitao Liu, Zhiteng Liu, Zhiwei Liu, Zhixiang Liu, Zhixue Liu, Zhiyan Liu, Zhiying Liu, Zhiyong Liu, Zhiyuan Liu, Zhong Liu, Zhong Wu Liu, Zhong-Hua Liu, Zhong-Min Liu, Zhong-Qiu Liu, Zhong-Wu Liu, Zhong-Ying Liu, Zhongchun Liu, Zhongguo Liu, Zhonghua Liu, Zhongjian Liu, Zhongjuan Liu, Zhongmin Liu, Zhongqi Liu, Zhongqiu Liu, Zhongwei Liu, Zhongyu Liu, Zhongyue Liu, Zhongzhong Liu, Zhou Liu, Zhou-di Liu, Zhu Liu, Zhuangjun Liu, Zhuanhua Liu, Zhuo Liu, Zhuoyuan Liu, Zi Hao Liu, Zi-Hao Liu, Zi-Lun Liu, Zi-Ye Liu, Zi-wen Liu, Zichuan Liu, Zihang Liu, Zihao Liu, Zihe Liu, Ziheng Liu, Zijia Liu, Zijian Liu, Zijing J Liu, Zimeng Liu, Ziqian Liu, Ziqin Liu, Ziteng Liu, Zitian Liu, Ziwei Liu, Zixi Liu, Zixuan Liu, Ziyang Liu, Ziying Liu, Ziyou Liu, Ziyuan Liu, Ziyue Liu, Zong-Chao Liu, Zong-Yuan Liu, Zonghua Liu, Zongjun Liu, Zongtao Liu, Zongxiang Liu, Zu-Guo Liu, Zuguo Liu, Zuohua Liu, Zuojin Liu, Zuolu Liu, Zuyi Liu, Zuyun Liu
articles

Genome-wide variation study and inter-tissue communication analysis unveil regulatory mechanisms of egg-laying performance in chickens.

Dandan Wang, Lizhi Tan, Yihao Zhi +20 more · 2024 · Nature communications · Nature · added 2026-04-24
Egg-laying performance is of great economic importance in poultry, but the underlying genetic mechanisms are still elusive. In this work, we conduct a multi-omics and multi-tissue integrative study in Show more
Egg-laying performance is of great economic importance in poultry, but the underlying genetic mechanisms are still elusive. In this work, we conduct a multi-omics and multi-tissue integrative study in hens with distinct egg production, to detect the hub candidate genes and construct hub molecular networks contributing to egg-laying phenotypic differences. We identifiy three hub candidate genes as egg-laying facilitators: TFPI2, which promotes the GnRH secretion in hypothalamic neuron cells; CAMK2D, which promotes the FSHβ and LHβ secretion in pituitary cells; and OSTN, which promotes granulosa cell proliferation and the synthesis of sex steroid hormones. We reveal key endocrine factors involving egg production by inter-tissue crosstalk analysis, and demonstrate that both a hepatokine, APOA4, and an adipokine, ANGPTL2, could increase egg production by inter-tissue communication with hypothalamic-pituitary-ovarian axis. Together, These results reveal the molecular mechanisms of multi-tissue coordinative regulation of chicken egg-laying performance and provide key insights to avian reproductive regulation. Show less
📄 PDF DOI: 10.1038/s41467-024-50809-9
APOA4

PPARα is one of the key targets for dendrobine to improve hepatic steatosis in NAFLD.

Yanzhe Xu, Miao Wang, Yi Luo +4 more · 2024 · Journal of ethnopharmacology · Elsevier · added 2026-04-24
Dendrobium nobile Lindl. (DNL) is a traditional Chinese ethnobotanical herb. Dendrobine (DNE) has been designated as a quality indicator for DNL in the Chinese Pharmacopoeia. DNE exhibits various phar Show more
Dendrobium nobile Lindl. (DNL) is a traditional Chinese ethnobotanical herb. Dendrobine (DNE) has been designated as a quality indicator for DNL in the Chinese Pharmacopoeia. DNE exhibits various pharmacological activities, including the reduction of blood lipids, regulation of blood sugar levels, as well as anti-inflammatory and antioxidant properties. The objective of this study is to explore the impact of DNE on lipid degeneration in nonalcoholic fatty liver disease (NAFLD) liver cells and elucidate its specific mechanism. The findings aim to offer theoretical support for the development of drugs related to DNL. We utilized male C57BL/6J mice, aged 6 weeks old, to establish a NAFLD model. This model allowed us to assess the impact of DNE on liver pathology and lipid levels in NAFLD mice. We investigated the mechanism of DNE's regulation of lipid metabolism through RNA-seq analysis. Furthermore, a NAFLD model was established using HepG2 cells to further evaluate the impact of DNE on the pathological changes of NAFLD liver cells. The potential mechanism of DNE's improvement was rapidly elucidated using HT-qPCR technology. These results were subsequently validated using mouse liver samples. Following the in vitro activation or inhibition of PPARα function, we observed changes in DNE's ability to ameliorate pathological changes in NAFLD hepatocytes. This mechanism was further verified through RT-qPCR and Western blot analysis. DNE demonstrated a capacity to enhance serum TC, TG, and liver TG levels in mice, concurrently mitigating liver lipid degeneration. RNA-seq analysis unveiled that DNE primarily modulates the expression of genes related to metabolic pathways in mouse liver. Utilizing HT-qPCR technology, it was observed that DNE markedly regulates the expression of genes associated with the PPAR signaling pathway in liver cells. Consistency was observed in the in vivo data, where DNE significantly up-regulated the expression of PPARα mRNA and its protein level in mouse liver. Additionally, the expression of fatty acid metabolism-related genes (ACOX1, CPT2, HMGCS2, LPL), regulated by PPARα, was significantly elevated following DNE treatment. In vitro experiments further demonstrated that DNE notably ameliorated lipid deposition, peroxidation, and inflammation levels in NAFLD hepatocytes, particularly when administered in conjunction with fenofibrate. Notably, the PPARα inhibitor GW6471 attenuated these effects of DNE. In summary, DNE exerts its influence on the expression of genes associated with downstream fat metabolism by regulating PPARα. This regulatory mechanism enhances liver lipid metabolism, mitigates lipid degeneration in hepatocytes, and ultimately ameliorates the pathological changes in NAFLD hepatocytes. Show less
no PDF DOI: 10.1016/j.jep.2023.117684
LPL

Exposome-Wide Ranking to Uncover Environmental Chemicals Associated with Dyslipidemia: A Panel Study in Healthy Older Chinese Adults from the BAPE Study.

Enmin Ding, Fuchang Deng, Jianlong Fang +23 more · 2024 · Environmental health perspectives · added 2026-04-24
Environmental contaminants (ECs) are increasingly recognized as crucial drivers of dyslipidemia and cardiovascular disease (CVD), but the comprehensive impact spectrum and interlinking mechanisms rema Show more
Environmental contaminants (ECs) are increasingly recognized as crucial drivers of dyslipidemia and cardiovascular disease (CVD), but the comprehensive impact spectrum and interlinking mechanisms remain uncertain. We aimed to systematically evaluate the association between exposure to 80 ECs across seven divergent categories and markers of dyslipidemia and investigate their underpinning biomolecular mechanisms via an unbiased integrative approach of internal chemical exposome and multi-omics. A longitudinal study involving 76 healthy older adults was conducted in Jinan, China, and participants were followed five times from 10 September 2018 to 19 January 2019 in 1-month intervals. A broad spectrum of seven chemical categories covering the prototypes and metabolites of 102 ECs in serum or urine as well as six serum dyslipidemia markers [total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, apolipoprotein (Apo)A1, ApoB, and ApoE4] were measured. Multi-omics, including the blood transcriptome, serum/urine metabolome, and serum lipidome, were profiled concurrently. Exposome-wide association study and the deletion/substitution/addition algorithms were applied to explore the associations between 80 EC exposures detection frequency Eight main ECs [1-naphthalene, 1-pyrene, 2-fluorene, dibutyl phosphate, tri-phenyl phosphate, mono-(2-ethyl-5-hydroxyhexyl) phthalate, chromium, and vanadium] were significantly associated with most dyslipidemia markers. Multi-omics indicated that the associations were mediated by endogenous biomolecules and pathways, primarily pertinent to CVD, inflammation, and metabolism. Clinical measures of cytokines and electrocardiograms further cross-validated the association of these exogenous ECs with systemic inflammation and cardiac function, demonstrating their potential mechanisms in driving dyslipidemia pathogenesis. It is imperative to prioritize mitigating exposure to these ECs in the primary prevention and control of the dyslipidemia epidemic. https://doi.org/10.1289/EHP13864. Show less
📄 PDF DOI: 10.1289/EHP13864
APOB

Targeted Knockdown of Hepatic Δ-5 Fatty Acid Desaturase FADS1 Aggravates Atherosclerosis in ApoE

Qiulei Liu, Peng Wang, Zhao Yang +2 more · 2024 · Frontiers in bioscience (Landmark edition) · added 2026-04-24
The endogenous metabolism of polyunsaturated fatty acids is regulated by the fatty acid desaturase (FADS) gene cluster and is strongly associated with diseases such as atherosclerosis, dyslipidemia, a Show more
The endogenous metabolism of polyunsaturated fatty acids is regulated by the fatty acid desaturase (FADS) gene cluster and is strongly associated with diseases such as atherosclerosis, dyslipidemia, and type 2 diabetes. However, the association between FADS and atherosclerosis remains a subject of debate. In this study, we specifically investigated the physiological role of Δ-5 fatty acid desaturase (FADS1) in aortic and peripheral vessel (namely, the femoral artery) atherosclerosis by targeting the selective knockdown of hepatic Knockdown of hepatic Our study demonstrated that knockdown of hepatic Show less
no PDF DOI: 10.31083/j.fbl2904131
FADS1

Apolipoprotein A-IV restrains fat accumulation in skeletal and myocardial muscles by inhibiting lipogenesis and activating PI3K-AKT signalling.

Wenqian Zhang, Xiao-Huan Liu, Jin-Ting Zhou +4 more · 2024 · Archives of physiology and biochemistry · Taylor & Francis · added 2026-04-24
One of the pathological characteristics of obesity is fat accumulation of skeletal muscles (SKM) and the myocardium, involving mechanisms of insulin resistance and abnormal lipid metabolism. Apolipopr Show more
One of the pathological characteristics of obesity is fat accumulation of skeletal muscles (SKM) and the myocardium, involving mechanisms of insulin resistance and abnormal lipid metabolism. Apolipoprotein A-IV (ApoA-IV) is an essential gene in both glucose and lipid metabolisms. Using high-fat diet (HFD) induced obese In stable obese animal models, we find ApoA-IV-knockout mice show elevated TG content, enhanced expression of lipogenic enzymes and diminished phosphorylated AKT in SKM and the myocardium, but both stable hepatic expression of AAV- We find that ApoA-IV reduces fat accumulation by suppressing lipogenesis and improves glucose uptake in SKM and the myocardium by regulating the PI3K-AKT pathway. Show less
no PDF DOI: 10.1080/13813455.2022.2163261
APOA4

Exploring the causal effect between lipid-modifying drugs and idiopathic pulmonary fibrosis: a drug-target Mendelian randomization study.

Gexiang Cai, Jingjing Liu, Mengsi Cai +1 more · 2024 · Lipids in health and disease · BioMed Central · added 2026-04-24
Idiopathic pulmonary fibrosis (IPF) is a respiratory disorder of obscure etiology and limited treatment options, possibly linked to dysregulation in lipid metabolism. While several observational studi Show more
Idiopathic pulmonary fibrosis (IPF) is a respiratory disorder of obscure etiology and limited treatment options, possibly linked to dysregulation in lipid metabolism. While several observational studies suggest that lipid-lowering agents may decrease the risk of IPF, the evidence is inconsistent. The present Mendelian randomization (MR) study aims to determine the association between circulating lipid traits and IPF and to assess the potential influence of lipid-modifying medications for IPF. Summary statistics of 5 lipid traits (high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglyceride, apolipoprotein A, and apolipoprotein B) and IPF were sourced from the UK Biobank and FinnGen Project Round 10. The study's focus on lipid-regulatory genes encompassed PCSK9, NPC1L1, ABCG5, ABCG8, HMGCR, APOB, LDLR, CETP, ANGPTL3, APOC3, LPL, and PPARA. The primary effect estimates were determined using the inverse-variance-weighted method, with additional analyses employing the contamination mixture method, robust adjusted profile score, the weighted median, weighted mode methods, and MR-Egger. Summary-data-based Mendelian randomization (SMR) was used to confirm significant lipid-modifying drug targets, leveraging data on expressed quantitative trait loci in relevant tissues. Sensitivity analyses included assessments of heterogeneity, horizontal pleiotropy, and leave-one-out methods. There was no significant effect of blood lipid traits on IPF risk (all P＞0.05). Drug-target MR analysis indicated that genetic mimicry for inhibitor of NPC1L1, PCSK9, ABCG5, ABCG8, and APOC3 were associated with increased IPF risks, with odds ratios (ORs) and 95% confidence intervals (CIs) as follows: 2.74 (1.05-7.12, P = 0.039), 1.36 (1.02-1.82, P = 0.037), 1.66 (1.12-2.45, P = 0.011), 1.68 (1.14-2.48, P = 0.009), and 1.42 (1.20-1.67, P = 3.17×10 Serum lipid traits did not significantly affect the risk of idiopathic pulmonary fibrosis. Drug targets MR studies examining 12 lipid-modifying drugs indicated that PCSK9 inhibitors could dramatically increase IPF risk, a mechanism that may differ from their lipid-lowering actions and thus warrants further investigation. Show less
📄 PDF DOI: 10.1186/s12944-024-02218-6
APOB

A

Yalu Cui, Wenping Xu, Jinpei Liu +6 more · 2024 · Genes & diseases · Elsevier · added 2026-04-24
📄 PDF DOI: 10.1016/j.gendis.2023.02.042
BBS4

Helicobacter pylori-Induced Angiopoietin-Like 4 Promotes Gastric Bacterial Colonization and Gastritis.

Rui Xie, Nan You, Wan-Yan Chen +21 more · 2024 · Research (Washington, D.C.) · added 2026-04-24
📄 PDF DOI: 10.34133/research.0409
ANGPTL4

Identification and validation of SHC1 and FGFR1 as novel immune-related oxidative stress biomarkers of non-obstructive azoospermia.

Yang Pan, Xiangyu Chen, Hang Zhou +7 more · 2024 · Frontiers in endocrinology · Frontiers · added 2026-04-24
Non-obstructive azoospermia (NOA) is a major contributor of male infertility. Herein, we used existing datasets to identify novel biomarkers for the diagnosis and prognosis of NOA, which could have gr Show more
Non-obstructive azoospermia (NOA) is a major contributor of male infertility. Herein, we used existing datasets to identify novel biomarkers for the diagnosis and prognosis of NOA, which could have great significance in the field of male infertility. NOA datasets were obtained from the Gene Expression Omnibus (GEO) database. CIBERSORT was utilized to analyze the distributions of 22 immune cell populations. Hub genes were identified by applying weighted gene co-expression network analysis (WGCNA), machine learning methods, and protein-protein interaction (PPI) network analysis. The expression of hub genes was verified in external datasets and was assessed by receiver operating characteristic (ROC) curve analysis. Gene set enrichment analysis (GSEA) was applied to explore the important functions and pathways of hub genes. The mRNA-microRNA (miRNA)-transcription factors (TFs) regulatory network and potential drugs were predicted based on hub genes. Single-cell RNA sequencing data from the testes of patients with NOA were applied for analyzing the distribution of hub genes in single-cell clusters. Furthermore, testis tissue samples were obtained from patients with NOA and obstructive azoospermia (OA) who underwent testicular biopsy. RT-PCR and Western blot were used to validate hub gene expression. Two immune-related oxidative stress hub genes ( It appears that Show less
📄 PDF DOI: 10.3389/fendo.2024.1356959
FGFR1

A Critical Functional Missense Mutation (T117M) in Sheep

Ziyi Zhao, Yuta Yang, Peiyao Liu +5 more · 2024 · Animals : an open access journal from MDPI · MDPI · added 2026-04-24
The melanocortin 4 receptor (
📄 PDF DOI: 10.3390/ani14152207
MC4R

TNKS1BP1 facilitates ubiquitination of CNOT4 by TRIM21 to promote hepatocellular carcinoma progression and immune evasion.

Yuan Wang, Ineza Karambizi Sandrine, Li Ma +9 more · 2024 · Cell death & disease · Nature · added 2026-04-24
Immune checkpoint inhibitors, particularly PD-1/PD-L1 blockades, have been approved for unresectable hepatocellular carcinoma (HCC). However, high resistance rates still limit their efficacy, highligh Show more
Immune checkpoint inhibitors, particularly PD-1/PD-L1 blockades, have been approved for unresectable hepatocellular carcinoma (HCC). However, high resistance rates still limit their efficacy, highlighting the urgent need to understand the underlying mechanisms and develop strategies for overcoming the resistance. In this study, tankyrasel binding protein 1 (TNKS1BP1) was found to interact with tripartite motif containing 21 (TRIM21) and mediated the ubiquitination of CCR4-NOT transcription complex subunit 4 (CNOT4) at the K239 residue via K48 and K6 linkage, which was essential for its tumorigenesis function. Autophagy and lipid reprogramming were identified as two possible mechanisms underlying the pro-tumor effect of TNKS1BP1. Upregulated TNKS1BP1 inhibited autophagy while induced lipid accumulation by inhibiting the JAK2/STAT3 pathway upon the degradation of CNOT4 in HCC. Importantly, knocking down TNKS1BP1 synergized with anti-PD-L1 treatment by upregulating PD-L1 expression on tumor cells via the JAK2/STAT3 pathway, and remodeling the tumor microenvironment by increasing infiltration of tumor-infiltrating lymphocytes as well as augmenting the effect of cytotoxic T lymphocytes. In conclusion, this study identified TNKS1BP1 as a predictive biomarker for patient prognosis and a promising therapeutic target to overcome anti-PD-L1 resistance in HCC. Show less
no PDF DOI: 10.1038/s41419-024-06897-y
TNKS1BP1

Molecular mechanisms of hypothalamic-pituitary-ovarian/thyroid axis regulating age at first egg in geese.

Zhiyu He, Qingyuan Ouyang, Qingliang Chen +7 more · 2024 · Poultry science · Elsevier · added 2026-04-24
Age at first egg (AFE) has consistently garnered interest as a crucial reproductive indicator within poultry production. Previous studies have elucidated the involvement of the hypothalamic-pituitary- Show more
Age at first egg (AFE) has consistently garnered interest as a crucial reproductive indicator within poultry production. Previous studies have elucidated the involvement of the hypothalamic-pituitary-ovarian (HPO) and hypothalamic-pituitary-thyroid (HPT) axes in regulating poultry sexual maturity. Concurrently, there was evidence suggesting a potential co-regulatory relationship between these 2 axes. However, as of now, no comprehensive exploration of the key pathways and genes responsible for the crosstalk between the HPO and HPT axes in the regulation of AFE has been reported. In this study, we conducted a comparative analysis of morphological differences and performed transcriptomic analysis on the hypothalamus, pituitary, thyroid, and ovarian stroma between normal laying group (NG) and abnormal laying group (AG). Morphological results showed that the thyroid index difference (D-) value (thyroid index D-value=right thyroid index-left thyroid index) was significantly (P < 0.05) lower in the NG than in the AG, while the ovarian index was significantly (P < 0.01) higher in the NG than in the AG. Furthermore, between NG and AG, we identified 99, 415, 167, and 1182 differentially expressed genes (DEGs) in the hypothalamus, pituitary, thyroid, and ovarian stroma, respectively. Gene ontology (GO) analysis highlighted that DEGs from 4 tissues were predominantly enriched in the "biological processes" category. Additionally, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that 16, 14, 3, and 26 KEGG pathways were significantly enriched (P < 0.05) in the hypothalamus, pituitary, thyroid, and ovarian stroma. The MAPK signaling pathway emerged as the sole enriched pathway across all 4 tissues. Employing an integrated analysis of the protein-protein interaction (PPI) network and correlation analysis, we found GREB1 emerged as a pivotal component within the HPO axis to regulate estrogen-related signaling in the HPT axis, meanwhile, the HPT axis influenced ovarian development by regulating thyroid hormone-related signaling mainly through OPN5. Then, 10 potential candidate genes were identified, namely IGF1, JUN, ERBB4, KDR, PGF, FGFR1, GREB1, OPN5, DIO3, and THRB. These findings establish a foundation for elucidating the physiological and genetic mechanisms by which the HPO and HPT axes co-regulate goose AFE. Show less
📄 PDF DOI: 10.1016/j.psj.2024.103478
FGFR1

Attenuation of high-fat diet-induced weight gain by apolipoprotein A4.

Hsuan-Chih N Kuo, Zachary LaRussa, Flora Mengyang Xu +7 more · 2024 · Obesity (Silver Spring, Md.) · Wiley · added 2026-04-24
Apolipoprotein A4 (APOA4) is synthesized by the small intestine in response to dietary lipids. Chronic exposure to a high-fat diet (HFD) desensitizes lipid-induced APOA4 production and attenuates brow Show more
Apolipoprotein A4 (APOA4) is synthesized by the small intestine in response to dietary lipids. Chronic exposure to a high-fat diet (HFD) desensitizes lipid-induced APOA4 production and attenuates brown adipose tissue (BAT) thermogenesis. We hypothesized that exogenous APOA4 could increase BAT thermogenesis and energy expenditure in HFD-fed mice, resulting in decreased obesity and improved glucose tolerance. BAT and inguinal white adipose tissue (IWAT) thermogenesis, body composition, energy intake and expenditure, and locomotor activity were measured using an infrared camera, immunoblots, quantitative magnetic resonance imaging, and a comprehensive lab animal monitoring system. An intraperitoneal glucose tolerance test and hepatic lipid accumulation and steatosis were assayed. Mice receiving continuous infusion of APOA4 for the last 4 weeks of 10 weeks of HFD feeding gained no additional body weight and had reduced fat mass but enhanced BAT and IWAT thermogenesis and energy expenditure, despite unaltered food intake and locomotor activity. Additionally, APOA4 infusion elevated fatty acid β oxidation; decreased lipogenesis, lipid accumulation, and steatosis in liver; and improved glucose tolerance. Maintenance of plasma APOA4 via exogenous APOA4 protein parallels elevation of BAT and IWAT thermogenesis, hepatic fatty acid β oxidation, and overall energy expenditure, with subsequent prevention of additional weight gain in HFD-fed obese mice. Show less
📄 PDF DOI: 10.1002/oby.24155
APOA4

Metformin promotes anti-tumor immunity in

Zhiguo Wang, Kunlin Li, Conghua Lu +12 more · 2024 · Oncology research · added 2026-04-24
Metformin has pleiotropic effects beyond glucose reduction, including tumor inhibition and immune regulation. It enhanced the anti-tumor effects of programmed cell death protein 1 (PD-1) inhibitors in Show more
Metformin has pleiotropic effects beyond glucose reduction, including tumor inhibition and immune regulation. It enhanced the anti-tumor effects of programmed cell death protein 1 (PD-1) inhibitors in serine/threonine kinase 11 ( We performed untargeted metabolomics using liquid chromatography (LC)-mass spectrometry (MS)/MS system and conducted cell experiments to verify the results of bioinformatics analysis. According to the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway database, most metabolites were annotated into metabolism, including nucleotide metabolism. Next, the differentially expressed metabolites in H460 (refers to H460 cells), H460_met (refers to metformin-treated H460 cells), and H460_KO_met (refers to metformin-treated Relying on AXIN1, metformin upregulated multiple nucleotide metabolites which promoted STING signaling and the killing of activated T cells in Show less
📄 PDF DOI: 10.32604/or.2024.052664
AXIN1

Penalized Regression Based Proteome-Wide Association Study Reveals Potential Population-Specific Drug Targets for Alzheimer's Disease in European and African American Cohorts.

Shuo Shi, Shijun Liu, You Liu +1 more · 2024 · AMIA ... Annual Symposium proceedings. AMIA Symposium · added 2026-04-24
Alzheimer's disease (AD) is a complex neurodegenerative disorder with significant genetic underpinnings, yet effective treatments remain elusive. To bridge the gap between genetic discoveries and ther Show more
Alzheimer's disease (AD) is a complex neurodegenerative disorder with significant genetic underpinnings, yet effective treatments remain elusive. To bridge the gap between genetic discoveries and therapeutic development, we conducted a penalized regression based proteome-wide association study (PWAS) in both European and African American populations. Using publicly available GWAS summary statistics and the BLISS model, we identified 37 protein-coding genes significantly associated with AD risk, including APOE and BCAM in both populations. We further applied the GREP model to prioritize repositionable drugs targeting these genes, identifying 30 significant disease-target-drug pairs. Notably, Ramipril and BAY 85-8501 emerged as top candidates for AD treatment in European and African American populations, respectively. These findings highlight ancestry-specific drug targets, demonstrating the importance of diverse genetic studies in AD research and providing novel avenues for therapeutic intervention. Show less
no PDF DOI: 10.1001/archpsyc.63.2.168
APOE

Exploring DIX-DIX Homo- and Hetero-Oligomers in Wnt Signaling with AlphaFold2.

Zehua Wen, Lei Wang, Shi-Wei Liu +3 more · 2024 · Cells · MDPI · added 2026-04-24
Wnt signaling is involved in embryo development and cancer. The binding between the DIX domains of Axin1/2, Dishevelled1/2/3, and Coiled-coil-DIX1 is essential for Wnt/β-catenin signaling. Structural Show more
Wnt signaling is involved in embryo development and cancer. The binding between the DIX domains of Axin1/2, Dishevelled1/2/3, and Coiled-coil-DIX1 is essential for Wnt/β-catenin signaling. Structural and biological studies have revealed that DIX domains are polymerized through head-to-tail interface interactions, which are indispensable for activating β-catenin Wnt signaling. Although different isoforms of Dvl and Axin proteins display both redundant and specific functions in Wnt signaling, the specificity of DIX-mediated interactions remains unclear due to technical challenges. Using AlphaFold2(AF2), we predict the structures of 6 homodimers and 22 heterodimers of DIX domains without templates and compare them with the reported X-ray complex structures. PRODIGY is used to calculate the binding affinities of these DIX complexes. Our results show that the Axin2 DIX homodimer has a stronger binding affinity than the Axin1 DIX homodimer. Among Dishevelled (Dvl) proteins, the binding affinity of the Dvl1 DIX homodimer is stronger than that of Dvl2 and Dvl3. The Coiled-coil-DIX1(Ccd1) DIX homodimer shows weaker binding than the Axin1 DIX homodimer. Generally, heterodimer interactions tend to be stronger than those of homodimers. Our findings provide insights into the mechanism of the Wnt signaling pathway and highlight the potential of AF2 and PRODIGY for studying protein-protein interactions in signaling pathways. Show less
📄 PDF DOI: 10.3390/cells13191646
AXIN1

1-Naphthaleneacetic Acid Improved the In Vitro Cell Culturing by Inhibiting Apoptosis.

Zhongyi Wang, Fengqi Li, Chunjing Feng +9 more · 2024 · Advanced biology · Wiley · added 2026-04-24
In vitro cell culturing witnessed its applications in scientific research and industrial activities. Attempts to shorten the doubling time of cultured cells have never ceased. In plants, auxin is appl Show more
In vitro cell culturing witnessed its applications in scientific research and industrial activities. Attempts to shorten the doubling time of cultured cells have never ceased. In plants, auxin is applied to promote plant growth, the synthetic derivative 1-Naphthaleneacetic acid (NAA) is a good example. Despite the auxin's naturally occurring receptors are not present in mammalian cells, studies suggested they may affect cell culturing. Yet the effects and mechanisms are still unclear. Here, an up to 2-fold increase in the yield of in vitro cultured human cells is observed. Different types of human cell lines and primary cells are tested and found that NAA is effective in all the cells tested. The PI staining followed by FACS suggested that NAA do not affect the cell cycling. Apoptosis-specific dye staining analysis implicated that NAA rescued cell death. Further bulk RNA sequencing is done and it is identified that the lipid metabolism-engaging and anti-apoptosis gene, ANGPTL4, is enhanced in expression upon NAA treatment. Studies on ANGPTL4 knockout cells indicated that ANGPTL4 is required for NAA-mediated response. Thus, the data identified a beneficial role of NAA in human cell culturing and highlighted its potency in in vitro cell culturing. Show less
no PDF DOI: 10.1002/adbi.202300593
ANGPTL4

Clinicopathologic features and outcomes of acute leukemia harboring PICALM::MLLT10 fusion.

Jeffrey Wang, Weiwei Zhang, Xinjie Xu +13 more · 2024 · Human pathology · Elsevier · added 2026-04-24
The PICALM::MLLT10 fusion is a rare but recurrent cytogenetic abnormality in acute leukemia, with limited clinicopathologic and outcome data available. Herein, we analyzed 156 acute leukemia patients Show more
The PICALM::MLLT10 fusion is a rare but recurrent cytogenetic abnormality in acute leukemia, with limited clinicopathologic and outcome data available. Herein, we analyzed 156 acute leukemia patients with PICALM::MLLT10 fusion, including 12 patients from our institutions and 144 patients from the literature. The PICALM::MLLT10 fusion preferentially manifested in pediatric and young adult patients, with a median age of 24 years. T-lymphoblastic leukemia/lymphoma (T-ALL) constituted 65% of cases, acute myeloid leukemia (AML) 27%, and acute leukemia of ambiguous lineage (ALAL) 8%. About half of T-ALL were classified as an early T-precursor (ETP)-ALL. In our institutions' cohort, mediastinum was the most common extramedullary site of involvement. Eight of 12 patients were diagnosed with T-ALL exhibiting a pro-/pre-T stage phenotype (CD4/CD8-double negative, CD7-positive), and frequent CD79a expression. NGS revealed pathogenic mutations in 5 of 6 tested cases, including NOTCH1, and genes in RAS and JAK-STAT pathways and epigenetic modifiers. Of 138 cases with follow-up, pediatric patients (<18 years) had 5-year overall survival (OS) of 71%, significantly better than adults at 33%. The 5-year OS for AML patients was 25%, notably shorter than T-ALL patients at 54%; this distinction was observed in both pediatric and adult populations. Furthermore, adult but not pediatric ETP-ALL patients demonstrated inferior survival compared to non-ETP-ALL patients. Neither karyotype complexity nor transplant status had a discernible impact on OS. In conclusion, PICALM::MLLT10 fusion is most commonly seen in T-ALL patients, particularly those with an ETP phenotype. AML and adult ETP-ALL patients had adverse prognosis. PICALM::MLTT10 fusion testing should be considered in T-ALL, AML, and ALAL patients. Show less
no PDF DOI: 10.1016/j.humpath.2024.07.003
MLLT10

Anti-miR-141-3p maintains homeostasis between autophagy and apoptosis by targeting Yy1 in the fetal lumbosacral defecation center of rats.

Yue Li, Peiqi Liu, Yifan Yao +5 more · 2024 · Molecular therapy. Nucleic acids · Elsevier · added 2026-04-24
Anorectal malformations (ARMs) are congenital diseases that lead to postoperative fecal incontinence, constipation, and soiling, despite improvements in surgery; however, their pathological mechanisms Show more
Anorectal malformations (ARMs) are congenital diseases that lead to postoperative fecal incontinence, constipation, and soiling, despite improvements in surgery; however, their pathological mechanisms remain unclear. Here, we report the role of microRNA-141-3p in maintaining homeostasis between apoptosis and autophagy in the lumbosacral defecation center of fetal rats with ARMs. Elevated microRNA-141-3p expression inhibited YIN-YANG-1 expression by binding its 3' UTR, and repressed autophagy and triggered apoptosis simultaneously. Then, adenylate cyclase 3 was screened to be the downstream target gene of YIN-YANG-1 by chromatin immunoprecipitation sequencing experiments, and Yin Yang 1 could positively activate the transcription of adenylate cyclase 3 by directly interacting with the motif GAGATGG and ATGG in its promoter. Intraamniotic microinjection of adeno-rno-microRNA-141-3p-sponge-GFP in fetal rats with ARMs on embryonic day 15 restored apoptosis-autophagy homeostasis. These findings reveal that microRNA-141-3p upregulation impaired homeostasis between apoptosis and autophagy by inhibiting the YIN-YANG-1/adenylate cyclase 3 axis, and that intraamniotic injection of anti-microRNA-141-3p helped maintain homeostasis in the lumbosacral defecation center of ARMs during embryogenesis. Show less
📄 PDF DOI: 10.1016/j.omtn.2024.102163
ADCY3

The autocrine action of salidroside on osteoclast during osteoclastogenesis via hypoxia-inducible factor-1

Yutong Jin, Zhengyang Li, Lin Qi +7 more · 2024 · Human & experimental toxicology · SAGE Publications · added 2026-04-24
The objective of this study was to investigate the potential of salidroside (SAL) (a major active compound in The expression of HIF-1 SAL enhanced the expression of HIF-1 SAL promotes osteoclast proli Show more
The objective of this study was to investigate the potential of salidroside (SAL) (a major active compound in The expression of HIF-1 SAL enhanced the expression of HIF-1 SAL promotes osteoclast proliferation, differentiation and bone resorption through HIF-1 Show less
no PDF DOI: 10.1177/09603271241269028
ANGPTL4

Case report:

Zhulin Wang, Chunyao Huang, Wenbo Fan +6 more · 2024 · Frontiers in oncology · Frontiers · added 2026-04-24
Given their good antitumor effects, epidermal growth factor receptor (
📄 PDF DOI: 10.3389/fonc.2024.1347282
MACF1

ZPR1 is an immunodiagnostic biomarker and promotes tumor progression in esophageal squamous cell carcinoma.

Guiying Sun, Hua Ye, Huijuan Liu +8 more · 2024 · Cancer science · Blackwell Publishing · added 2026-04-24
To evaluate the potential of zinc finger protein 1 (ZPR1) as a diagnostic biomarker and explore the underlying role for esophageal squamous cell carcinoma (ESCC). A human proteome microarray was custo Show more
To evaluate the potential of zinc finger protein 1 (ZPR1) as a diagnostic biomarker and explore the underlying role for esophageal squamous cell carcinoma (ESCC). A human proteome microarray was customized to identify anti-ZPR1 autoantibody, and enzyme-linked immunosorbent assay (ELISA) was adopted to assess the diagnostic performance of anti-ZPR1 autoantibody in 294 patients with ESCC and 294 normal controls. The expression of ZPR1 protein was measured by immunohistochemistry. The effect of ZPR1 on the proliferation, migration, and invasion of ESCC cells was investigated through CCK-8, wound healing, and Transwell assays. The expression level of anti-ZPR1 autoantibody (fold change = 2.77) in ESCC patients was higher than that in normal controls. The receiver operating characteristic (ROC) analysis manifested anti-ZPR1 autoantibody achieved area under the ROC curve (AUC) of 0.726 and 0.734 to distinguish ESCC from normal controls with sensitivity of 50.0% and 42.3%, and specificity of 91.0% and 92.0% in the test group and validation group, respectively. The positive rate of ZPR1 protein was significantly higher in ESCC tissues (75.5%, 80/106) than paracancerous tissues (9.4%, 5/53). Compared with the human normal esophageal cell line, the expression level of ZPR1 mRNA and protein in ESCC lines (KYSE150, Eca109, and TE1) had an increased trend. The knockdown or overexpression of ZPR1 reduced and enhanced the proliferation, migration, and invasion of ESCC cell, respectively. ZPR1 was a potential immunodiagnostic biomarker for noninvasive detection and could be a promotional factor in tumor progression of ESCC. Show less
no PDF DOI: 10.1111/cas.16004
ZPR1

Adipose tissue peroxisomal lipid synthesis orchestrates obesity and insulin resistance through LXR-dependent lipogenesis.

Brian Kleiboeker, Anyuan He, Min Tan +8 more · 2024 · Molecular metabolism · Elsevier · added 2026-04-24
Adipose tissue mass is maintained by a balance between lipolysis and lipid storage. The contribution of adipose tissue lipogenesis to fat mass, especially in the setting of high-fat feeding, is consid Show more
Adipose tissue mass is maintained by a balance between lipolysis and lipid storage. The contribution of adipose tissue lipogenesis to fat mass, especially in the setting of high-fat feeding, is considered minor. Here we investigated the effect of adipose-specific inactivation of the peroxisomal lipid synthetic protein PexRAP on fatty acid synthase (FASN)-mediated lipogenesis and its impact on adiposity and metabolic homeostasis. To explore the role of PexRAP in adipose tissue, we metabolically phenotyped mice with adipose-specific knockout of PexRAP. Bulk RNA sequencing was used to determine transcriptomic responses to PexRAP deletion and Adipose-specific PexRAP deletion promoted diet-induced obesity and insulin resistance through activation of de novo lipogenesis. Mechanistically, PexRAP inactivation inhibited the flux of carbons to ethanolamine plasmalogens. This increased the nuclear PC/PE ratio and promoted cholesterol mislocalization, resulting in activation of liver X receptor (LXR), a nuclear receptor known to be activated by increased intracellular cholesterol. LXR activation led to increased expression of the phospholipid remodeling enzyme LPCAT3 and induced FASN-mediated lipogenesis, which promoted diet-induced obesity and insulin resistance. These studies reveal an unexpected role for peroxisome-derived lipids in regulating LXR-dependent lipogenesis and suggest that activation of lipogenesis, combined with dietary lipid overload, exacerbates obesity and metabolic dysregulation. Show less
no PDF DOI: 10.1016/j.molmet.2024.101913
NR1H3

AAV-mediated hepatic LPL expression ameliorates severe hypertriglyceridemia and acute pancreatitis in Gpihbp1 deficient mice and rats.

Chenchen Yuan, Yao Xu, Guotao Lu +12 more · 2024 · Molecular therapy : the journal of the American Society of Gene Therapy · Elsevier · added 2026-04-24
GPIHBP1 plays an important role in the hydrolysis of triglyceride (TG) lipoproteins by lipoprotein lipases (LPLs). However, Gpihbp1 knockout mice did not develop hypertriglyceridemia (HTG) during the Show more
GPIHBP1 plays an important role in the hydrolysis of triglyceride (TG) lipoproteins by lipoprotein lipases (LPLs). However, Gpihbp1 knockout mice did not develop hypertriglyceridemia (HTG) during the suckling period but developed severe HTG after weaning on a chow diet. It has been postulated that LPL expression in the liver of suckling mice may be involved. To determine whether hepatic LPL expression could correct severe HTG in Gpihbp1 deficiency, liver-targeted LPL expression was achieved via intravenous administration of the adeno-associated virus (AAV)-human LPL gene, and the effects of AAV-LPL on HTG and HTG-related acute pancreatitis (HTG-AP) were observed. Suckling Gpihbp1 Show less
📄 PDF DOI: 10.1016/j.ymthe.2023.11.018
LPL

Clinicopathological analysis of rosette-forming glioneuronal tumors.

Jing Liu, Fan Lin, Yanhua Sun +1 more · 2024 · Diagnostic pathology · BioMed Central · added 2026-04-24
This study aimed to investigate the clinicopathological characteristics, diagnostic indicators, and critical factors for the differential diagnosis of rosette-forming glioneuronal tumor (RGNT). This r Show more
This study aimed to investigate the clinicopathological characteristics, diagnostic indicators, and critical factors for the differential diagnosis of rosette-forming glioneuronal tumor (RGNT). This retrospective study included six surgically treated RGNT cases. We analyzed and summarized their clinical manifestations, radiological features, histological morphology, immunophenotype, and molecular genetic changes, supplemented with a literature review. The patients comprised four males and two females with a mean age of 35 years. The tumors were located in the cerebellum (two cases); the fourth ventricle, quadrigeminal cistern, and third ventricle (one case each); and the fourth ventricle and brainstem (one case). Clinical manifestations included headaches in four cases, left eyelid ptosis in one case, and one asymptomatic case only identified during physical examination. Microscopically, the tumor cells were uniform in size and were marked by rosette-like or pseudorosette-like structures around the neuropil and blood vessels. Immunohistochemistry revealed biphasic patterns. The central neuropil components of the rosette-like structures around the neuropil and the pseudorosette structures of the perivascular regions expressed Syn, while the cells surrounding the rosettes expressed Olig2 and not GFAP. GFAP and S-100 were expressed in the glial components but not in the rosette or pseudorosette regions. The Ki-67 proliferation index was typically low. Molecular genetic analysis showed that the main molecular changes involved FGFR1 mutation accompanied by PIK3R1 mutation. None of the patients received chemoradiotherapy postoperatively. Follow-up durations varied between 4 and 23 months with no recorded recurrence or metastasis. RGNT is a comparatively rare mixed glioneuronal tumor that occurs in the midline structures. Its morphology shows certain overlaps with other low-grade neuroepithelial tumors. Identifying the rosettes around the neuropil is critical for morphological diagnosis, and the molecular identification of FGFR1 mutations accompanied by PIK3R1 mutations can facilitate diagnosis. Show less
📄 PDF DOI: 10.1186/s13000-024-01465-6
FGFR1

Magnetic Resonance Imaging-Based Radiogenomic Analysis Reveals Genomic Determinants for Nanoparticle Delivery into Tumors.

Di Liu, Na Lu, Fengchao Zang +13 more · 2024 · ACS nano · ACS Publications · added 2026-04-24
Even though the enhanced permeability and retention (EPR) effect is applicable for the passive targeting of solid tumors, many nanodrugs have failed to achieve meaningful clinical outcomes due to the Show more
Even though the enhanced permeability and retention (EPR) effect is applicable for the passive targeting of solid tumors, many nanodrugs have failed to achieve meaningful clinical outcomes due to the heterogeneity of EPR effect. Therefore, understanding the mechanism of the EPR effect is crucial to overcome the obstacles nanomedicines face in clinical translation. The aim of this study was to establish a reliable method to increase awareness of the critical influencing factors of nanoparticle (NP) transport into tumors based on the EPR effect using a combined radiogenomics and clinical magnetic resonance imaging (MRI) technique and gene set pathway enrichment analysis. Employing poly(lactic- Show less
no PDF DOI: 10.1021/acsnano.4c09387
DLG2

Impact of rosuvastatin on metabolic syndrome patients with moderate to severe metabolic associated fatty liver disease without overt diabetes: A randomized clinical trial.

Xuan Wang, Lu Lyu, Wei Li +6 more · 2024 · Diabetes & metabolic syndrome · Elsevier · added 2026-04-24
This investigation aimed to evaluate the efficacy and safety of rosuvastatin in treating moderate to severe metabolic associated fatty liver disease (MAFLD). This prospective, open-label, randomized s Show more
This investigation aimed to evaluate the efficacy and safety of rosuvastatin in treating moderate to severe metabolic associated fatty liver disease (MAFLD). This prospective, open-label, randomized study included non-diabetic participants with metabolic syndrome and intrahepatocellular lipid (IHCL) levels >10 %, as determined by proton magnetic resonance spectroscopy ( Thirty-two participants completed the study. Rosuvastatin resulted in a significant absolute (△IHCL: 7.61 ± 4.51 vs. 1.54 ± 5.33, p = 0.002) and relative reduction in IHCL (△IHCL%: -42.28 ± 24.90 % vs. -8.91 ± 31.93 %, p = 0.003) compared to the control. Reduction in IHCL correlated significantly with decreases in low-density lipoprotein cholesterol (LDL-C) (r = 0.574, p < 0.01), apolipoprotein B (ApoB) (r = 0.660, p < 0.001), and free fatty acids (FFA) (r = 0.563, p = 0.005). No significant safety differences were observed between groups. Rosuvastatin significantly reduced hepatic steatosis in individuals with moderate to severe MAFLD and metabolic syndrome over 52 weeks, while maintaining a favorable safety profile. Show less
no PDF DOI: 10.1016/j.dsx.2024.103126
APOB

Social isolation impairs cognition via Aβ-mediated synaptic dysfunction.

Fang Huang, Xinghua Liu, Qian Guo +6 more · 2024 · Translational psychiatry · Nature · added 2026-04-24
Social isolation (SI) is a common phenomenon in the modern world, especially during the coronavirus disease 2019 pandemic, and causes lasting cognitive impairments and mental disorders. However, it is Show more
Social isolation (SI) is a common phenomenon in the modern world, especially during the coronavirus disease 2019 pandemic, and causes lasting cognitive impairments and mental disorders. However, it is still unclear how SI alters molecules in the brain and induces behavioural dysfunctions. Here, we report that SI impairs cognitive function and induces depressive-like behaviours in C57BL/6 J mice, in addition to impairing synaptic plasticity and increasing the levels of APP cleavage-related enzymes, thereby promoting Aβ production. Moreover, we show that in APP/PS1 transgenic mice, SI accelerates pathological changes and behavioural deficits. Interestingly, downregulation of the expression of the BACE1 attenuates SI-induced Aβ toxicity and synaptic dysfunction. Furthermore, early intervention with BACE1 shRNA blocks SI-induced cognitive impairments. Together, our data strongly suggest that SI-induced upregulation of BACE1 expression mediates Aβ toxicity and induces behavioural deficits. Down-regulation of BACE1 may be a promising strategy for preventing SI-induced cognitive impairments. Show less
📄 PDF DOI: 10.1038/s41398-024-03078-5
BACE1

BCKDH kinase promotes hepatic gluconeogenesis independent of BCKDHA.

Feiye Zhou, Chunxiang Sheng, Xiaoqin Ma +11 more · 2024 · Cell death & disease · Nature · added 2026-04-24
Elevated circulating branched-chain amino acids (BCAAs) are tightly linked to an increased risk in the development of type 2 diabetes mellitus. The rate limiting enzyme of BCAA catabolism branched-cha Show more
Elevated circulating branched-chain amino acids (BCAAs) are tightly linked to an increased risk in the development of type 2 diabetes mellitus. The rate limiting enzyme of BCAA catabolism branched-chain α-ketoacid dehydrogenase (BCKDH) is phosphorylated at E1α subunit (BCKDHA) by its kinase (BCKDK) and inactivated. Here, the liver-specific BCKDK or BCKDHA knockout mice displayed normal glucose tolerance and insulin sensitivity. However, knockout of BCKDK in the liver inhibited hepatic glucose production as well as the expression of key gluconeogenic enzymes. No abnormal gluconeogenesis was found in mice lacking hepatic BCKDHA. Consistent with the vivo results, BT2-mediated inhibition or genetic knockdown of BCKDK decreased hepatic glucose production and gluconeogenic gene expressions in primary mouse hepatocytes while BCKDK overexpression exhibited an opposite effect. Whereas, gluconeogenic gene expressions were not altered in BCKDHA-silenced hepatocytes. Mechanistically, BT2 treatment attenuated the interaction of cAMP response element binding protein (CREB) with CREB-binding protein and promoted FOXO1 protein degradation by increasing its ubiquitination. Our findings suggest that BCKDK regulates hepatic gluconeogenesis through CREB and FOXO1 signalings, independent of BCKDHA-mediated BCAA catabolism. Show less
📄 PDF DOI: 10.1038/s41419-024-07071-0
BCKDK

A novel FGFR1 inhibitor CYY292 suppresses tumor progression, invasion, and metastasis of glioblastoma by inhibiting the Akt/GSK3β/snail signaling axis.

Yanran Bi, Ruiling Zheng, Jiahao Hu +9 more · 2024 · Genes & diseases · Elsevier · added 2026-04-24
Glioblastoma (GBM) is a malignant brain tumor that grows quickly, spreads widely, and is resistant to treatment. Fibroblast growth factor receptor (FGFR)1 is a receptor tyrosine kinase that regulates Show more
Glioblastoma (GBM) is a malignant brain tumor that grows quickly, spreads widely, and is resistant to treatment. Fibroblast growth factor receptor (FGFR)1 is a receptor tyrosine kinase that regulates cellular processes, including proliferation, survival, migration, and differentiation. FGFR1 was predominantly expressed in GBM tissues, and FGFR1 expression was negatively correlated with overall survival. We rationally designed a novel small molecule CYY292, which exhibited a strong affinity for the FGFR1 protein in GBM cell lines Show less
📄 PDF DOI: 10.1016/j.gendis.2023.02.035
FGFR1