👤 Chengbi Xu

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Also published as: Ai-Guo Xu, Aili Xu, Aimin Xu, Aishi Xu, Aixiao Xu, Andrew Z Xu, Anlong Xu, Anqi Xu, Anton Xu, Aohong Xu, Aoling Xu, Bai-Hui Xu, Baijie Xu, Banglao Xu, Baofeng Xu, Baoping Xu, Bei Xu, Beibei Xu, Beisi Xu, Benhong Xu, Bi-Yun Xu, Biao Xu, Bilian Xu, Bilin Xu, Bin Xu, Bing Xu, Bing-E Xu, Bingfang Xu, Bingqi Xu, Bingqian Xu, Bingqing Xu, Bingxin Xu, Binqiang Xu, Bo Xu, Bocheng Xu, Bojie Xu, Boming Xu, Boqing Xu, C C Xu, C F Xu, Cai Xu, Caiqiu Xu, Caixia Xu, Carrie Xu, Chan Xu, Chang Xu, Chang-Qing Xu, Changde Xu, Changfu Xu, Changlin Xu, Changliu Xu, Changlu Xu, Changwu Xu, Chao Xu, Chaoguang Xu, Chaohua Xu, Chaoqun Xu, Chaoyu Xu, Chen Xu, Chen-Run Xu, Chen-Yang Xu, Cheng Xu, Cheng-Bin Xu, Cheng-Jian Xu, Chengkai Xu, Chengqi Xu, Chengxun Xu, Chengye Xu, Chengyun Xu, Chenhao Xu, Chenjie Xu, Chenqi Xu, Chentong Xu, Chong Xu, Chong-Feng Xu, Chuang Xu, Chuanrui Xu, Chun Xu, Chunhui Xu, Chunjie Xu, Chunlan Xu, Chunli Xu, Chunlin Xu, Chunming Xu, Chunwei Xu, Chunxiao Xu, Chunyan Xu, Chunyu Xu, Cian Xu, Cineng Xu, Cong Xu, Cong-jian Xu, Congjian Xu, Cun Xu, Cunshuan Xu, Cynthia M Xu, D Xu, D-J Xu, Da Xu, Da-Peng Xu, Daichao Xu, Daiqi Xu, Dan Xu, Dandan Xu, Danfeng Xu, Danning Xu, Danping Xu, Danyan Xu, Danyi Xu, Daohua Xu, Dapeng Xu, Daqian Xu, Dawei Xu, De Xu, De-Xiang Xu, Dequan Xu, Dexiang Xu, Di Xu, Di-Mei Xu, Dilin Xu, Ding Xu, Dong Xu, Dong-Hui Xu, Dong-Juan Xu, DongZhu Xu, Dongchen Xu, Donghang Xu, Dongju Xu, Dongjun Xu, Dongke Xu, Dongmei Xu, Enwei Xu, Erping Xu, F F Xu, F Xu, Fang Xu, Fang-Fang Xu, Fang-Yuan Xu, Fangfang Xu, Fanghua Xu, Fangmin Xu, Fangui Xu, Fei Xu, Feilai Xu, Fen Xu, Feng Xu, Feng-Qin Xu, Feng-Xia Xu, Feng-Yuan Xu, Fenghuang Xu, Fengqin Xu, Fengxia Xu, Fengyan Xu, Fengzhe Xu, Flora Mengyang Xu, Fu Xu, Fuyi Xu, G Xu, Gang Xu, Gangchun Xu, Gaosi Xu, Gaoyuan Xu, Genxing Xu, George X Xu, Geyang Xu, Gezhi Xu, Gu-Feng Xu, Guang Xu, Guang-Hong Xu, Guang-Qing Xu, Guanghao Xu, Guangquan Xu, Guangsen Xu, Guangwei Xu, Guangyan Xu, Guangyu Xu, Guanhua Xu, Guanlan Xu, Guanyi Xu, Gui-Ping Xu, Guifa Xu, Guiyun Xu, Guo Xu, Guo-Liang Xu, Guo-Tong Xu, Guo-Xing Xu, Guofeng Xu, Guogang Xu, Guoheng Xu, Guoliang Xu, Guoshuai Xu, Guowang Xu, Guoxu Xu, Guozheng Xu, H Eric Xu, H F Xu, H X Xu, H Y Xu, Haifeng Xu, Haijin Xu, Haikun Xu, Hailey Xu, Hailiang Xu, Haiman Xu, Haimin Xu, Haiming Xu, Haiqi Xu, Haixia Xu, Haixiang Xu, Haiyan Xu, Haiying Xu, Han Xu, Hanchen Xu, Hanfei Xu, Hang Xu, Hanqian Xu, Hanting Xu, Hanyuan Xu, Hao Xu, Haoda Xu, Haonan Xu, Haowen Xu, Haoyang Xu, Haoyu Xu, Heng Xu, Hengyi Xu, Heping Xu, Hong Xu, Hong-Yan Xu, Hong-tao Xu, Hong-wei Xu, Hongbei Xu, Hongbo Xu, Hongen Xu, Hongfa Xu, Hongjian Xu, Hongjiang Xu, Hongle Xu, Hongli Xu, Honglin Xu, Hongmei Xu, Hongming Xu, Hongrong Xu, Hongtao Xu, Hongwei Xu, Hongwen Xu, Hongxia Xu, Hongyan Xu, Hongzhi Xu, Houguo Xu, Houxi Xu, Hu Xu, Hua Xu, Huaisha Xu, Huaiyuan Xu, Huajun Xu, Huan Xu, Huaxiang Xu, Hui Ming Xu, Hui Xu, Hui-Lian Xu, HuiTing Xu, Huihui Xu, Huimian Xu, Huiming Xu, Huiqiong Xu, Huixuan Xu, Iris M J Xu, J T Xu, J Xu, Janfeng Xu, Jason Xu, Jia Xu, Jia-Chen Xu, Jia-Li Xu, Jia-Mei Xu, Jia-Xin Xu, Jia-Yue Xu, Jiaai Xu, Jiacheng Xu, Jiachi Xu, Jiahong Xu, Jiahui Xu, Jiajia Xu, Jiajie Xu, Jiake Xu, Jiali Xu, Jialin Xu, Jialu Xu, Jiaming Xu, Jian Hua Xu, Jian Xu, Jian-Guang Xu, Jiancheng Xu, Jianfeng Xu, Jiang Xu, Jiangang Xu, Jianguang Xu, Jianguo Xu, Jianhua Xu, Jianing Xu, Jianjuan Xu, Jianliang Xu, Jianming Xu, Jianping Xu, Jianqiu Xu, Jianwei Xu, Jianxin Xu, Jianyong Xu, Jianzhong Xu, Jiapei Xu, Jiapeng Xu, Jiaqi Xu, Jiaqian Xu, Jiaqin Xu, Jiawei Xu, Jiaying Xu, Jiayunzhu Xu, Jie Xu, Jie-Hua Xu, Jiean Xu, Jielin Xu, Jin Xu, Jinchao Xu, Jinfeng Xu, Jing Xu, Jing-Yi Xu, Jing-Ying Xu, Jing-Yu Xu, Jinghong Xu, Jinghua Xu, Jingjie Xu, Jingjing Xu, Jingjun Xu, Jinguo Xu, Jingya Xu, Jingyi Xu, Jingying Xu, Jingyu Xu, Jingzhou Xu, Jinhe Xu, Jinhua Xu, Jinjian Xu, Jinjie Xu, Jinjin Xu, Jinsheng Xu, Jinshu Xu, Jinsong Xu, Jinxian Xu, Jinxin Xu, Jinyi Xu, Jinying Xu, Jinyu Xu, Jinyuan Xu, Jishu Xu, Jixuan Xu, Jiyi Xu, Jiyu Xu, Julie Xu, Jun Xu, Jun-Chao Xu, Junchang Xu, Junfei Xu, Junfeng Xu, Junjie Xu, Junnv Xu, Kai Xu, Kaihao Xu, Kailian Xu, Kaishou Xu, Kaixiang Xu, Kaiyue Xu, Ke Xu, Keke Xu, Keli Xu, Kelin Xu, Keman Xu, Keshu Xu, Kewei Xu, Kexin Xu, Keyun Xu, Kuanfeng Xu, Kun Xu, L Xu, Laizhi Xu, Lanjin Xu, Lei Xu, Leilei Xu, Leisheng Xu, Leiting Xu, Leiyu Xu, Leyuan Xu, Li Xu, Li-Jun Xu, Li-Li Xu, Li-Ling Xu, Li-Wei Xu, Li-Yan Xu, Li-Zhi Xu, Lian-Wei Xu, Liang Xu, Lianjun Xu, Libin Xu, Lichi Xu, Lidan Xu, Lifen Xu, Lihui Xu, Lijiao Xu, Lijuan Xu, Lijun Xu, Lili Xu, Limin Xu, Lin Xu, Ling Xu, Lingjuan Xu, Lingli Xu, Lingling Xu, Lingna Xu, Lingxiang Xu, Lingyan Xu, Lingyang Xu, Lingyao Xu, Lingyi Xu, Linna Xu, Linyan Xu, Liping Xu, Liqun Xu, Lisha Xu, Lisi Xu, Liu Xu, Liwen Xu, Liyi Xu, Long Xu, Longfei Xu, Longsheng Xu, Lu Xu, Lu-Lu Xu, Lubin Xu, Lun-Shan Xu, Luyi Xu, M Xu, M-Y Xu, Mai Xu, Man Xu, Manman Xu, Manyi Xu, Mao Xu, Maochang Xu, Maodou Xu, Maotian Xu, Mei Xu, Mei-Jun Xu, Meifang Xu, Meifeng Xu, Meishu Xu, Meixi Xu, Meiyu Xu, Meng Xu, Mengjie Xu, Mengjun Xu, Mengmeng Xu, Mengping Xu, Mengqi Xu, Mengru Xu, Mengsi Xu, Mengyi Xu, Mengying Xu, Mengyue Xu, Miao Xu, Miaomiao Xu, Min Jie Xu, Min Xu, Min-Xuan Xu, Ming Xu, Ming-Jiang Xu, Ming-Zhu Xu, Mingcong Xu, Minghao Xu, Minghong Xu, Mingjie Xu, Minglan Xu, Mingli Xu, Mingliang Xu, Mingming Xu, Mingqian Xu, Mingyuan Xu, Mingzhu Xu, Minxuan Xu, Mu Xu, N Y Xu, Nan Xu, Nannan Xu, Nathan Xu, Nenggui Xu, Ning Xu, Ning'an Xu, Ningda Xu, Nong Xu, Nuo Xu, Pan Xu, Panpan Xu, Pao Xu, Peidi Xu, Peigang Xu, Peiwei Xu, Peiyu Xu, Peng Xu, Peng-Ju Xu, Peng-Yuan Xu, Pengfei Xu, Penghui Xu, Pengjie Xu, Pengli Xu, Pin-Xian Xu, Ping Xu, Pingwen Xu, Pu Xu, Q P Xu, Qi Xu, Qi-Qi Xu, Qian Xu, Qian-Fei Xu, Qianghua Xu, Qianhui Xu, Qianlan Xu, Qianqian Xu, Qianzhu Xu, Qiaoshi Xu, Qihang Xu, Qikui Xu, Qiming Xu, Qin Xu, Qin-Zhi Xu, Qing Xu, Qing-Wen Xu, Qing-Yang Xu, Qingchan Xu, Qingheng Xu, Qinghua Xu, Qingjia Xu, Qingqing Xu, Qingqiu Xu, Qingwen Xu, Qingxia Xu, Qingyuan Xu, Qinli Xu, Qinwen Xu, Qiong Xu, Qiongying Xu, Qiu-Han Xu, Qiuhong Xu, Qiuhui Xu, Qiulin Xu, Qiushi Xu, Qiuyu Xu, Qiuyue Xu, Qiuyun Xu, Quanzhong Xu, Ran Xu, Rang Xu, Ren Xu, Ren-He Xu, Renfang Xu, Renshi Xu, Renyuan Xu, Richard H Xu, Rong Xu, Rongbin Xu, Rongrong Xu, Rongying Xu, Ru-xiang Xu, Rui Xu, Rui-Hua Xu, Rui-Ming Xu, Rui-Xia Xu, Ruifeng Xu, Ruiling Xu, Run-Xiang Xu, Runhao Xu, Ruohong Xu, Ruonan Xu, Ruxiang Xu, S Xu, Shan Xu, Shan-Rong Xu, Shan-Shan Xu, Shang-Fu Xu, Shang-Rong Xu, Shanhai Xu, Shanqi Xu, Shanqiang Xu, Shanshan Xu, Shaonian Xu, Shaoqi Xu, Shendong Xu, Sheng-Qian Xu, Shengen Xu, Shengjie Xu, Shengtao Xu, Shengyu Xu, Shi-Na Xu, Shihao Xu, Shihui Xu, Shiliyang Xu, Shimeng Xu, Shiqing Xu, Shiwen Xu, Shiyao Sherrie Xu, Shiyi Xu, Shiyun Xu, Shoujia Xu, Shu-Xian Xu, Shu-Zhen Xu, Shuai Xu, Shuaili Xu, Shuang Xu, Shuangbing Xu, Shude Xu, Shufen Xu, Shuhua Xu, Shuiyang Xu, Shujing Xu, Shun Xu, Shunjiang Xu, Shuqia Xu, Shutao Xu, Shuwan Xu, Shuwen Xu, Shuxiang Xu, Sifan Xu, Sihua Xu, Siqun Xu, Song Xu, Song-Hui Xu, Song-Song Xu, Songli Xu, Songsong Xu, Steven Jing-Liang Xu, Suling Xu, Suo-Wen Xu, Suowen Xu, Suoyu Xu, Sutong Xu, T Xu, Tan Xu, Tao Xu, Tengfei Xu, Tengxiao Xu, Tengyun Xu, Tian Xu, Tian-Le Xu, Tian-Rui Xu, Tian-Ying Xu, TianBo Xu, Tiancheng Xu, Tianfeng Xu, Tianli Xu, Tianmin Xu, Tiantian Xu, Tianxiang Xu, Tianyi Xu, Tianyu Xu, Tieshan Xu, Ting Xu, Ting-Xin Xu, Tingting Xu, Tingxuan Xu, Tong Xu, Tongda Xu, Tonghong Xu, Tongtong Xu, Tongxin Xu, Tongyang Xu, W M Xu, W W Xu, W Xu, Wan-Ting Xu, Wancheng Xu, Waner Xu, Wanfu Xu, Wang-Dong Xu, Wang-Hong Xu, Wangdong Xu, Wanhai Xu, Wanqi Xu, Wanting Xu, Wanwan Xu, Wanxue Xu, Wei Xu, Weide Xu, Weidong Xu, Weifeng Xu, Weihai Xu, Weihong Xu, Weijie Xu, Weilan Xu, Weili Xu, Weiming Xu, Weiqun Xu, Weixia Xu, Weiyong Xu, Weizhi Xu, Wen Xu, Wen-Hao Xu, Wen-Hui Xu, Wen-Juan Xu, Wen-Xiong Xu, Wenbin Xu, Wenchun Xu, Wenhao Xu, Wenhuan Xu, Wenhui Xu, Wenjie Xu, Wenjing Xu, Wenjuan Xu, Wenjun Xu, Wenlong Xu, Wenming Xu, Wenping Xu, Wenqi Xu, Wenqing Xu, Wentao Xu, Wenwen Xu, Wenwu Xu, Wenxin Xu, Wenxuan Xu, Wenyan Xu, Wenyuan Xu, Wenzhuo Xu, X S Xu, X Xu, Xia Xu, Xia-Jing Xu, Xiang Xu, Xiang-Min Xu, Xiang-liang Xu, Xiangbin Xu, Xianghong Xu, Xiangshan Xu, Xiangyu Xu, Xianli Xu, Xiao Le Xu, Xiao Xu, Xiao-Dan Xu, Xiao-Hua Xu, Xiao-Hui Xu, Xiao-Lin Xu, Xiao-Shan Xu, Xiaobo Xu, Xiaocheng Xu, Xiaofang Xu, Xiaofeng Xu, Xiaoge Xu, Xiaohan Xu, Xiaohong Ruby Xu, Xiaohui Xu, Xiaojiang Xu, Xiaojiao Xu, Xiaojin Xu, Xiaojing Xu, Xiaojuan Xu, Xiaojun Xu, Xiaoke Xu, Xiaolei Xu, Xiaoli Xu, Xiaolin Xu, Xiaolong Xu, Xiaolu Xu, Xiaomeng Xu, Xiaoming Xu, Xiaopeng Xu, Xiaoqin Xu, Xiaoshuang Xu, Xiaotao Xu, Xiaoting Xu, Xiaowen Xu, Xiaowu Xu, Xiaoya Xu, Xiaoyan Xu, Xiaoyang Xu, Xiaoyin Xu, Xiaoyu Xu, Xiayun Xu, Xihui Xu, Xin Xu, Xin-Rong Xu, Xingmeng Xu, Xingsheng Xu, Xingshun Xu, Xingyan Xu, Xingyu Xu, Xingzhi Xu, Xinjie Xu, Xinxuan Xu, Xinyi Xu, Xinyin Xu, Xinyu Xu, Xinyuan Xu, Xinyue Xu, Xinyun Xu, Xiongfei Xu, Xiqi Xu, Xirui Xu, Xiufeng Xu, Xizhan Xu, Xizheng Xu, Xu Xu, Xuan Xu, Xuanqi Xu, Xuegong Xu, Xuejin Xu, Xuejun Xu, Xueni Xu, Xun Xu, Xuting Xu, Y Xu, Ya'nan Xu, Ya-Nan Xu, Ya-Peng Xu, Ya-Ru Xu, Ya-lin Xu, Yali Xu, Yaling Xu, Yan Xu, YanFeng Xu, Yana Xu, Yanan Xu, Yanchang Xu, Yancheng Xu, Yanfei Xu, Yang Xu, Yangbin Xu, Yangliu Xu, Yangxian Xu, Yangyang Xu, Yanjun Xu, Yanli Xu, Yanling Xu, Yanming Xu, Yanni Xu, Yanqi Xu, Yanquan Xu, Yanwu Xu, Yanyan Xu, Yanyang Xu, Yanyong Xu, Yanzhe Xu, Yao Xu, Yaobo Xu, Yaowen Xu, Yaozeng Xu, Yaping Xu, Yaqi Xu, Yaqin Xu, Yaru Xu, Yawei Xu, Yayun Xu, Ye Xu, Yechun Xu, Yeqiu Xu, Yetao Xu, Yi Ran Xu, Yi Xu, Yi-Huan Xu, Yi-Liang Xu, Yi-Ni Xu, Yi-Tong Xu, Yi-Xian Xu, Yibin Xu, Yichi Xu, Yidan Xu, Yifan Xu, Yifeng Xu, Yigang Xu, Yihua Xu, Yimeng Xu, Yiming Xu, Yin Xu, Yinfeng Xu, Ying Xu, Yingju Xu, Yingli Xu, Yinglin Xu, Yingna Xu, Yingqianxi Xu, Yingzheng Xu, Yinhe Xu, Yinjie Xu, Yinli Xu, Yinxia Xu, Yinying Xu, Yiquan Xu, Yiting Xu, Yitong Xu, Yixin Xu, Yiyi Xu, Yong Xu, Yong-Nan Xu, Yongfeng Xu, Yongjian Xu, Yongmei Xu, Yongqing Xu, Yongsheng Xu, Yongsong Xu, You-Song Xu, Youjia Xu, Youping Xu, Youzhi Xu, Yu Xu, Yu-Fen Xu, Yu-Ming Xu, Yu-Peng Xu, Yu-Ping Xu, Yu-Xin Xu, Yuan Xu, Yuanfeng Xu, Yuanhong Xu, Yuanwei Xu, Yuanyuan Xu, Yuanzhi Xu, Yuanzhong Xu, Yubin Xu, Yuchen Xu, Yucheng Xu, Yue Xu, Yuejuan Xu, Yuerong Xu, Yuexin Xu, Yuexuan Xu, Yueyue Xu, Yuhan Xu, Yuheng Xu, Yujie Xu, Yuli Xu, Yuling Xu, Yun Xu, Yun-Teng Xu, Yunfang Xu, Yunfei Xu, Yungen Xu, Yunhe Xu, Yunjian Xu, Yunxi Xu, Yunxuan Xu, Yunyi Xu, Yuping Xu, Yurui Xu, Yushan Xu, Yuting Xu, Yuxiang Xu, Yuyang Xu, Yuzhen Xu, Yuzhi Xu, Yuzhong Xu, Z Xu, Zaibin Xu, Zaihua Xu, Zaikun Xu, Zaoyi Xu, Ze-Jun Xu, Zeao Xu, Zebang Xu, Zefeng Xu, Zejun Xu, Zekuan Xu, Zelin Xu, Zengliang Xu, Zeqing Xu, Zesheng Xu, Zetan Xu, Zeya Xu, Zeyu Xu, Zhan Xu, Zhanchi Xu, Zhanqiong Xu, Zhanyu Xu, Zhaofa Xu, Zhaojun Xu, Zhaoyao Xu, Zhe Xu, Zhen-Guo Xu, Zheng Xu, Zheng-Fan Xu, Zheng-Hong Xu, Zhengang Xu, Zhengshui Xu, Zhenming Xu, Zhenyu Xu, Zhenzhou Xu, Zhi Ping Xu, Zhi Xu, Zhi-Feng Xu, Zhi-Qing David Xu, Zhi-Zhen Xu, Zhicheng Xu, Zhidong Xu, Zhigang Xu, Zhihua Xu, Zhijie Xu, Zhiliang Xu, Zhilong Xu, Zhipeng Xu, Zhiqiang Xu, Zhiru Xu, Zhiting Xu, Zhiwei Xu, Zhixian Xu, Zhiyang Xu, Zhiyao Xu, Zhizhen Xu, Zhong Xu, Zhong-Hua Xu, Zhonghui Xu, Zhongwei Xu, Zhuangzhuang Xu, Zhunan Xu, Zi-Hua Xu, Zi-Xiang Xu, Zichuan Xu, Zifan Xu, Zihao Xu, Zihe Xu, Zihua Xu, Ziqi Xu, Ziwei Xu, Zixuan Xu, Ziyang Xu, Ziye Xu, Ziyu Xu, Zongli Xu, Zongren Xu, Zongzhen Xu, Zuojun Xu, Zuyuan Xu
articles

Clinical value of serum IL-27 in allergic rhinitis patients and its relationship with Treg associated cytokine levels.

Tiantian Xu, Yifei Yang · 2023 · Human immunology · Elsevier · added 2026-04-24
Allergic rhinitis (AR) is a nasal allergic disease mainly mediated by IgE, and the immune response is the pathological basis of AR pathogenesis. Regulatory T cells (Treg) has been confirmed to be invo Show more
Allergic rhinitis (AR) is a nasal allergic disease mainly mediated by IgE, and the immune response is the pathological basis of AR pathogenesis. Regulatory T cells (Treg) has been confirmed to be involved in the occurrence of AR. IL-27 mediates inflammatory responses and allergic symptoms in AR by promoting Tregs and related factors. Our study aimed to explore the correlation between serum interleukin 27 (IL-27) and Treg associated cytokines in the pathogenesis of AR. Based on the inclusion and exclusion criteria, 69 participants with AR and 50 healthy participants were selected. Their IL-27, IL-10, and TGF-β1 levels were estimated by ELISA. Receiver operating characteristics curve (ROC) was performed to demonstrate the diagnostic efficiency of IL-27 in AR. Pearson correlation analysis was used for correlation analysis. IL-27 in AR patients statistically decreased compared to the control group. Consistently, IL-27 were also negatively correlated with the clinical severity of AR patients. Treg related cytokines including IL-10 and TGF-β1 in AR patients was statistically decreased. In addition, the IL-10 and TGF-β1expressions were positively correlated with IL-27 in AR patients. IL-27 was statistically down-regulated in patients with AR, which is related to insufficient Treg function. Restoring the expression of IL-27 may become a novel approach to treat AR. Show less
no PDF DOI: 10.1016/j.humimm.2022.10.007
IL27

Deciphering the genetic architecture of atrial fibrillation offers insights into disease prediction, pathophysiology and downstream sequelae.

Shuai Yuan, Yuying Li, Lijuan Wang +13 more · 2023 · medRxiv : the preprint server for health sciences · Cold Spring Harbor Laboratory · added 2026-04-24
The study aimed to discover novel genetic loci for atrial fibrillation (AF), explore the shared genetic etiologies between AF and other cardiovascular and cardiometabolic traits, and uncover AF pathog Show more
The study aimed to discover novel genetic loci for atrial fibrillation (AF), explore the shared genetic etiologies between AF and other cardiovascular and cardiometabolic traits, and uncover AF pathogenesis using Mendelian randomization analysis. We conducted a genome-wide association study meta-analysis including 109,787 AF cases and 1,165,920 controls of European ancestry and identified 215 loci, among which 91 were novel. We performed Genomic Structural Equation Modeling analysis between AF and four cardiovascular comorbidities (coronary artery disease, ischemic stroke, heart failure, and vneous thromboembolism) and found 189 loci shared across these diseases as well as a universal genetic locus shared by atherosclerotic outcomes (i.e., rs1537373 near This genome-wide association study and trans-omic Mendelian randomization analysis provides insights into disease risk prediction, pathophysiology and downstream sequelae. Show less
📄 PDF DOI: 10.1101/2023.07.20.23292938
JMJD1C

JMJD1C promotes smooth muscle cell proliferation by activating glycolysis in pulmonary arterial hypertension.

Chen Zhang, Yue Sun, Yingying Guo +2 more · 2023 · Cell death discovery · Nature · added 2026-04-24
Pulmonary arterial hypertension (PAH) is a chronic disorder characterized by hyperproliferation of pulmonary arterial smooth muscle cells (PASMCs). JMJD1C, a member of the Jumonji domain containing C Show more
Pulmonary arterial hypertension (PAH) is a chronic disorder characterized by hyperproliferation of pulmonary arterial smooth muscle cells (PASMCs). JMJD1C, a member of the Jumonji domain containing C (JMJC) histone demethylase family, contributes to cardiovascular dysfunction. However, the role of JMJD1C in PAH remains unknown. Mice were exposed to hypoxia to mimic several features associated with PAH clinically. We found that JMJD1C was highly expressed in the lungs of mice after hypoxia exposure. JMJD1C knockdown ameliorated hypoxia-induced right ventricular remodeling and thickening of the pulmonary arterial wall. PASMC hyperproliferation and resistance to apoptosis in mice exposed to hypoxia were suppressed by JMJD1C inhibition. We demonstrated that JMJD1C silencing reduced glycolytic enzymes (HK2, PGK1 and LDHA) and lactate overaccumulation in the lungs of mice exposed to hypoxia. In vitro, hypoxia-induced hyperproliferation and activated glycolytic processes in mouse PASMCs were impaired by JMJD1C knockdown. In addition, the activation of STAT3 signaling by hypoxia was suppressed by JMJD1C silencing both in vivo and in vitro. The overexpression of STAT3 reversed the inhibitory effect of JMJD1C depletion on proliferation and glycolysis in PASMCs under hypoxia. Thus, JMJD1C induces glycolytic processes by activating STAT3 signaling to promote PASMC proliferation and pulmonary vascular remodeling, suggesting the potential role of JMJD1C in regulating the metabolic program and vascular remodeling in PAH. Show less
📄 PDF DOI: 10.1038/s41420-023-01390-5
JMJD1C

An alpha-helix variant p.Arg156Pro in LMNA as a cause of hereditary dilated cardiomyopathy: genetics and bioinfomatics exploration.

Lei Chang, Rong Huang, Jianzhou Chen +4 more · 2023 · BMC medical genomics · BioMed Central · added 2026-04-24
LMNA gene encodes lamin A/C protein which participates in the construction of nuclear lamina, the mutations of LMNA result in a wide variety of diseases known as laminopathies. LMNA-related dilated ca Show more
LMNA gene encodes lamin A/C protein which participates in the construction of nuclear lamina, the mutations of LMNA result in a wide variety of diseases known as laminopathies. LMNA-related dilated cardiomyopathy(LMNA-DCM) is one of the more common laminopathy which characterized by progressive heart failure and arrhythmia. However, the mutation features of LMNA-DCM are yet to be elucidated. Herein we described a dilated cardiomyopathy family carrying novel variant c.467G > C(p.Arg156Pro) of LMNA as heterozygous pathogenic variant identified by whole-exome sequencing. With the help of Alphafold2, we predicted mutant protein structure and found an interrupted α-helix region in lamin A/C. In the analysis of 49 confirmed pathogenic missense of laminopathies, Chi-square test showed the DCM phenotype was related to the α-helix region mutation (p < 0.017). After screening the differentially expressed genes (DEGs) in both mice models and human patients in Gene Expression Omnibus database, we found the variation of α-helix-coding region in LMNA caused abnormal transcriptomic features in cell migration, collagen-containing extracellular matrix, and PI3K-Akt signaling pathway. Subsequently we constructed (TF)-mRNA-microRNA (miRNA) regulatory network and identified 7 key genes (FMOD, CYP1B1, CA3, F2RL1, HAPLIN1, SNAP91, and KANSL1) as potential biomarkers or therapeutic targets in LMNA-DCM patients. Show less
📄 PDF DOI: 10.1186/s12920-023-01661-1
KANSL1

Shared Genetics and Comorbid Genes of Amyotrophic Lateral Sclerosis and Parkinson's Disease.

Ye Tian, Guochen Ma, Haoqi Li +7 more · 2023 · Movement disorders : official journal of the Movement Disorder Society · Wiley · added 2026-04-24
Comorbidity exists between amyotrophic lateral sclerosis (ALS) and Parkinson's disease (PD), but the role of genetic factors is unclear. We aim to investigate genetic correlation, causal relationship, Show more
Comorbidity exists between amyotrophic lateral sclerosis (ALS) and Parkinson's disease (PD), but the role of genetic factors is unclear. We aim to investigate genetic correlation, causal relationship, and comorbid genes between ALS and PD. Leveraging the largest genome-wide association study data (ALS: 27,205 cases, 110,881 controls; PDG: 33,674 cases, 449,056 controls), we used linkage disequilibrium score regression and Mendelian randomization analysis for genetic correlation and causal inference. We performed genome-wide cross-trait analysis via Multi-Trait Analysis of Genome-Wide Association Studies and Cross-Phenotype Association to identify specific single-nucleotide polymorphisms, followed by functional mapping and annotation. Integrating expression quantitative trait loci data from 13 brain regions, we conducted a transcriptome-wide association study via functional summary-based imputation and joint-tissue imputation to explore comorbid genes, followed by pathway enrichment analysis. We found that PD positively correlates with ALS (r Our work demonstrates shared genetic architecture between ALS and PD, reports new pleiotropic genes, and sheds light on the comorbid mechanism. © 2023 International Parkinson and Movement Disorder Society. Show less
no PDF DOI: 10.1002/mds.29572
KANSL1

Indolent B-cell lymphoma with t(14;19) investigated from a molecular perspective.

Jeremiah X Karrs, Shivaprasad H Sathyanarayana, Xinjie Xu +4 more · 2023 · Journal of hematopathology · Springer · added 2026-04-24
T(14;19) is an unusual but distinct genomic alteration reported in low-grade B-cell lymphomas. This structural rearrangement places BCL3 in juxtaposition with IGH inducing proliferation and has been f Show more
T(14;19) is an unusual but distinct genomic alteration reported in low-grade B-cell lymphomas. This structural rearrangement places BCL3 in juxtaposition with IGH inducing proliferation and has been found in chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), marginal zone lymphoma (MZL), and other low-grade B-cell lymphomas. While there are some case series describing this in the context of other cytogenetic alterations, there are limited clinical cases examined from a molecular perspective. We herein describe a case of a low-grade B-cell lymphoma with t(14;19) resulting in IGH::BCL3 fusion on which we performed whole exome sequencing to investigate genetic variants that could contribute to its pathogenesis. We found pathogenic alterations including a variant in CXCR4 which has been shown to be recurrently mutated in different low-grade B-cell lymphomas including lymphoplasmacytic lymphoma (LPL) and MZL. We describe this interesting case in the context of its genomic findings and how it contributes to the literature as a whole. Show less
📄 PDF DOI: 10.1007/s12308-023-00562-7
LPL

[miR-23b-3p regulates the differentiation of goat intramuscular preadipocytes by targeting the

Liyi Zhang, Xin Li, Qing Xu +5 more · 2023 · Sheng wu gong cheng xue bao = Chinese journal of biotechnology · added 2026-04-24
This study aimed to explore the effect of miR-23b-3p on the differentiation of goat intramuscular preadipocytes, and to confirm whether miR-23b-3p plays its roles
no PDF DOI: 10.13345/j.cjb.230156
LPL

Investigation of seasonal changes in lipid synthesis and metabolism-related genes in the oviduct of Chinese brown frog (Rana dybowskii).

Yankun Wang, Yuning Liu, Yawei Wang +5 more · 2023 · European journal of histochemistry : EJH · added 2026-04-24
A peculiar physiological characteristic of the Chinese brown frog (Rana dybowskii) is that its oviduct dilates during pre-brumation rather than during the breeding season. This research aimed to exami Show more
A peculiar physiological characteristic of the Chinese brown frog (Rana dybowskii) is that its oviduct dilates during pre-brumation rather than during the breeding season. This research aimed to examine the expression of genes connected with lipid synthesis and metabolism in the oviduct of R. dybowskii during both the breeding season and pre-brumation. We observed significant changes in the weight and size of the oviduct between the breeding season and pre-brumation. Furthermore, compared to the breeding season, pre-brumation exhibited significantly lower triglyceride content and a marked increase in free fatty acid content. Immunohistochemical results revealed the spatial distribution of triglyceride synthase (Dgat1), triglyceride hydrolase (Lpl and Hsl), fatty acid synthase (Fasn), and fatty acid oxidases (Cpt1a, Acadl, and Hadh) in oviductal glandular cells and epithelial cells during both the breeding season and pre-brumation. While the mRNA levels of triglycerides and free fatty acid synthesis genes (dgat1 and fasn) did not show a significant difference between the breeding season and pre-brumation, the mRNA levels of genes involved in triglycerides and free fatty acid metabolism (lpl, cpt1a, acadl, acox and hadh) were considerably higher during pre-brumation. Furthermore, the R. dybowskii oviduct's transcriptomic and metabolomic data confirmed differential expression of genes and metabolites enriched in lipid metabolism signaling pathways during both the breeding season and pre-brumation. Overall, these results suggest that alterations in lipid synthesis and metabolism during pre-brumation may potentially influence the expanding size of the oviduct, contributing to the successful overwintering of R. dybowskii. Show less
📄 PDF DOI: 10.4081/ejh.2023.3890
LPL

Loss-of-Function Homozygous Variant in

Hongyan Wu, Huan Xu, Song Lei +7 more · 2023 · Kidney international reports · Elsevier · added 2026-04-24
Lipoprotein lipase (LPL) is an important enzyme in lipid metabolism, individuals with Renal biopsy was conducted to confirm the etiological factor of nephrotic syndrome in a 44-year-old Chinese man. L Show more
Lipoprotein lipase (LPL) is an important enzyme in lipid metabolism, individuals with Renal biopsy was conducted to confirm the etiological factor of nephrotic syndrome in a 44-year-old Chinese man. Lipoprotein electrophoresis, Renal biopsy revealed numerous CD68 positive foam cells infiltrated in the glomeruli; immunoglobulin and complement staining were negative; and electron microscopy revealed numerous lipid droplets and cholesterol clefts in the cytoplasm of foam cells. Lipoprotein electrophoresis revealed that the patient fulfilled the diagnostic criteria of type I hyperlipoproteinemia. The apoE genotype of the patient was the ε3/ε3 genotype. Whole-exome sequencing revealed an Show less
📄 PDF DOI: 10.1016/j.ekir.2023.08.027
LPL

Combined exposure to deoxynivalenol facilitates lipid metabolism disorder in high-fat-diet-induced obesity mice.

Jing Jin, Bingxin Huangfu, Fuguo Xing +2 more · 2023 · Environment international · Elsevier · added 2026-04-24
Deoxynivalenol (DON) is a trichothecene toxin that mainly produced by strains of Fusarium spp. DON contamination is widely distributed and is a global food safety threat. Existing studies have expound Show more
Deoxynivalenol (DON) is a trichothecene toxin that mainly produced by strains of Fusarium spp. DON contamination is widely distributed and is a global food safety threat. Existing studies have expounded its harmful effects on growth inhibition, endocrine disruption, immune function impairment, and reproductive toxicity. In energy metabolism, DON suppresses appetite, reduces body weight, triggers lipid oxidation, and negatively affects cholesterol and fatty acid homeostasis. In this study, high-fat diet (HFD) induced obese C57BL/6J mice were orally treated with 0.1 mg/kg bw/d and 1.0 mg/kg bw/d DON for 4 weeks. The lipid metabolism of mice and the molecular mechanisms were explored. The data showed that although DON reduced body weight and fat mass in HFD mice, it significantly increased their serum triglyceride concentrations, disturbance of serum lipid metabolites, impaired glucose, and resulted in insulin intolerance in mice. In addition, the transcriptional and expression changes of lipid metabolism genes in the liver and epididymis (EP) adipose indicate that the DON-mediated increase in serum triglycerides is caused by lipoprotein lipase (LPL) inhibition in EP adipose. Furthermore, DON down-regulates the expression of LPL through the PPARγ signaling pathway in EP adipose. These results are further confirmed by the serum lipidomics analysis. In conclusion, DON acts on the PPARγ pathway of white adipose to inhibit the expression of LPL, mediate the increase of serum triglyceride in obese mice, disturb the homeostasis of lipid metabolism, and increase the risk of cardiovascular disease. This study reveals the interference mechanism of DON on lipid metabolism in obese mice and provides a theoretical basis for its toxic effect in obese individuals. Show less
no PDF DOI: 10.1016/j.envint.2023.108345
LPL

Effects of lysophospholipids and multi-enzymes on growth performance, antioxidant capacity, intestinal health, and cecal microflora of male cherry valley ducks.

Qianqian Zhang, Jian Li, Jianping Wang +8 more · 2023 · Journal of animal science · Oxford University Press · added 2026-04-24
Improvement of nutrient utilization to promote growth performance is always pursued in poultry. In this study, a total of 360 1-d-old male ducklings was randomly assigned to 3 treatments in terms of d Show more
Improvement of nutrient utilization to promote growth performance is always pursued in poultry. In this study, a total of 360 1-d-old male ducklings was randomly assigned to 3 treatments in terms of diet treatment groups. Three treatments were as follows: basal diet (Con group) or basal diet supplemented with 300 mg/kg multi-enzymes (ENZ group) or 500 mg/kg lysophospholipids (LPL group). On day 42, ducks were slaughtered for samplings. The results revealed that supplementary LPL improved the body weight (BW) at day 14 and average daily gain (ADG) during days 1 to 14 and improved the feed conversion rate (FCR) for the overall period (P < 0.05) by improving nutrient utilization of dry matter and ether extract (P < 0.05) compared with the Con group. Dietary ENZ improved the FCR from days 15-42 and 1-42, and nitrogen utilization (P < 0.05) compared with the Con group. Jejunal villus height and villus height/crypt depth ratio were higher (P < 0.05) in the LPL group and tended to be higher (P < 0.1) in the ENZ group compared to the Con group. Supplementation with either LPL or ENZ reduced interleukin-1β concentration in jejunal mucus (P < 0.05). Both LPL and ENZ enhanced serum total superoxide dismutase activity (P < 0.05), whereas only supplementation with LPL elevated total antioxidant capacity (P < 0.05). In terms of cecal microbiota, microbial richness tended to be reduced by LPL, with low observed-OTUs and Chao1 (0.05 < P < 0.1). Supplementation with ENZ led to higher abundances of cellulolytic bacteria such as Fibrobacterota, [Eubacterium]_xylanophilum_group, and Bifidobacterium. Overall, both LPL and ENZ improved FCR, which may be relevant to ameliorative intestinal health, overall antioxidant ability, and cecal microbiome. Show less
no PDF DOI: 10.1093/jas/skad361
LPL

Transcriptional Knock-down of mstn Encoding Myostatin Improves Muscle Quality of Nile Tilapia (Oreochromis niloticus).

Qingchun Wang, Yue Yan, Yifan Tao +3 more · 2023 · Marine biotechnology (New York, N.Y.) · Springer · added 2026-04-24
Myostatin (encoded by mstn) negatively regulates skeletal muscle mass and affects lipid metabolism. To explore the regulatory effects of mstn on muscle development and lipid metabolism in Nile tilapia Show more
Myostatin (encoded by mstn) negatively regulates skeletal muscle mass and affects lipid metabolism. To explore the regulatory effects of mstn on muscle development and lipid metabolism in Nile tilapia (Oreochromis niloticus), we used antisense RNA to transcriptionally knock-down mstn. At 180 days, the body weight and body length were significantly higher in the mstn-knock-down group than in the control group (p < 0.05). Additionally, fish with mstn-knock-down exhibited myofiber hyperplasia but not hypertrophy. Oil red O staining revealed a remarkable increase in the area of lipid droplets in muscle in the mstn-knockdown group (p < 0.05). Nutrient composition analyses of muscle tissue showed that the crude fat content was significantly increased in the mstn-knock-down group (p < 0.05). The contents of saturated fatty acids, monounsaturated fatty acids, and polyunsaturated fatty acids were all significantly increased in the mstn-knock-down group (p < 0.05). Comparative transcriptome analyses revealed 2420 significant differentially expressed genes between the mstn-knock-down group and the control group. KEGG analysis indicates that disruptions to fatty acid degradation, glycerolipid metabolism, and the PPAR signaling pathway affect muscle development and lipid metabolism in mstn-knock-down Nile tilapia: acaa2, eci1, and lepr were remarkably up-regulated, and acadvl, lpl, foxo3, myod1, myog, and myf5 were significantly down-regulated (p < 0.05). These results show that knock-down of mstn results in abnormal lipid metabolism, acceleration of skeletal muscle development, and increased adipogenesis and weight gain in Nile tilapia. Show less
📄 PDF DOI: 10.1007/s10126-023-10252-1
LPL

A scoring system based on fusion genes to predict treatment outcomes of the non-acute promyelocytic leukemia pediatric acute myeloid leukemia.

Wenwen Weng, Yanfei Chen, Yuwen Wang +8 more · 2023 · Frontiers in medicine · Frontiers · added 2026-04-24
Fusion genes are considered to be one of the major drivers behind cancer initiation and progression. Meanwhile, non-acute promyelocytic leukemia (APL) pediatric patients with acute myeloid leukemia (A Show more
Fusion genes are considered to be one of the major drivers behind cancer initiation and progression. Meanwhile, non-acute promyelocytic leukemia (APL) pediatric patients with acute myeloid leukemia (AML) in children had limited treatment efficacy. Hence, we developed and validated a simple clinical scoring system for predicting outcomes in non-APL pediatric patients with AML. A total of 184 non-APL pediatric patients with AML who were admitted to our hospital and an independent dataset (318 patients) from the TARGET database were included. Least absolute shrinkage and selection operation (LASSO) and Cox regression analysis were used to identify prognostic factors. Then, a nomogram score was developed to predict the 1, 3, and 5 years overall survival (OS) based on their clinical characteristics and fusion genes. The accuracy of the nomogram score was determined by calibration curves and receiver operating characteristic (ROC) curves. Additionally, an internal verification cohort was used to assess its applicability. Based on Cox and LASSO regression analyses, a nomogram score was constructed using clinical characteristics and OS-related fusion genes ( Our model based on the fusion gene is a prognostic biomarker for non-APL pediatric patients with AML. The nomogram score can provide personalized prognosis prediction, thereby benefiting clinical decision-making. Show less
📄 PDF DOI: 10.3389/fmed.2023.1258038
MLLT10

RNA sequencing of myeloid sarcoma, shed light on myeloid sarcoma stratification.

Yunfan Yang, Yang Shu, Yuan Tang +8 more · 2023 · Cancer medicine · Wiley · added 2026-04-24
Myeloid sarcoma (MS) is a rare, extramedullary tumor consisting of myeloid blasts. Little is known about the genetic background of MS and the prognostic value of genetic abnormalities in MS. In partic Show more
Myeloid sarcoma (MS) is a rare, extramedullary tumor consisting of myeloid blasts. Little is known about the genetic background of MS and the prognostic value of genetic abnormalities in MS. In particular, the broad variety of gene fusions that occur in MS is marginally covered by traditional testing methods due to lack of fresh tumor specimens. Here, we analyzed the clinical and genetic features of 61 MS cases. We performed RNA sequencing (RNA-seq) on formalin-fixed paraffin-embedded (FFPE) or fresh samples to analyze fusion genes in 26 cases. In addition, we performed genetic abnormalities-based risk stratification using fusion genes and gene mutations. A total of 305 fusion genes were identified in 22 cases, including the following five recurrent fusion genes: RUNX1-RUNX1T1, CBFβ-MYH11, ETV6-MECOM, FUS-ERG, and PICALM-MLLT10. The prognosis in the adverse-risk group was significantly worse than that in the favorable/intermediate-risk group (median survival: 12 months vs. not reached; p = 0.0004). These results indicated the efficacy of RNA-seq using FFPE-derived RNA as a clinical routine for detecting fusion genes, which can be used as markers for risk stratification in MS. Show less
📄 PDF DOI: 10.1002/cam4.5654
MLLT10

Mitocytosis Is Critical for Phthalate-Induced Injury to the Ovarian Granulosa Cell Layer in Quail (

Xiang-Yu Ma, Yu Zhu, Ya-Ru Xu +5 more · 2023 · Journal of agricultural and food chemistry · ACS Publications · added 2026-04-24
Phthalates are widely used synthetic chemicals that determine endocrine disruption effects on female reproductivity and oviposition. Our study demonstrated that the mitochondrial quality in ovarian gr Show more
Phthalates are widely used synthetic chemicals that determine endocrine disruption effects on female reproductivity and oviposition. Our study demonstrated that the mitochondrial quality in ovarian granulosa cells (GCs) is associated with a poor prognosis in female reproduction. However, the molecular mechanism of di-(2-ethylhexyl) phthalate (DEHP) exposure on the quail ovarian GC layer is still unknown. To validate the effects of DEHP on the GC layer, 8 days' old 150 female Japanese quail were treated orally with DEHP (250, 500, and 750 mg/kg BW/day) for 45 days to explore the toxic effects of DEHP on the ovarian GC layer. Histopathological assessment and ultrastructure observation found that DEHP decreased the thickness of the GC layer, resulted in mitochondrial damage, and activated mitocytosis. Additionally, the results further suggested that DEHP impacted the secretion of steroid hormones (reduced FSH, E2, and T levels and boosted Prog, PRL, and LH levels) by triggering mitocytosis (enhanced transcription of Show less
no PDF DOI: 10.1021/acs.jafc.2c08601
MYO19

Association of insulin signaling pathway

Xiang Xiao, Junxia Yan, Ning'an Xu +3 more · 2023 · Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · added 2026-04-24
Insulin signaling pathway plays an important role in metabolic associated fatty liver disease (MAFLD), however, the association between polymorphisms of genes related to insulin signaling pathway and Show more
Insulin signaling pathway plays an important role in metabolic associated fatty liver disease (MAFLD), however, the association between polymorphisms of genes related to insulin signaling pathway and MAFLD remains unclear. This study aims to investigate the association between insulin signaling pathway-related gene polymorphisms and gene-gene interactions with MAFLD susceptibility in obese children so as to provide scientific basis for further study of genetic mechanism. A total of 502 obese children with MAFLD who admitted to Hunan Provincial Children's Hospital from September 2019 to October 2021, were recruited as a case group, and 421 obese children with non-MAFLD admitted during the same period were recruited as a control group. Socio-demographic information, preterm birth history, eating habits, and exercise status of the subjects were collected by inquiry survey, and anthropometric information was collected by physical measurement. At the same time, 2 mL of venous blood was collected to extract DNA, and the polymorphism of insulin signaling pathway-related genes (5 representative candidate genes, 12 variants) was detected. Multivariate Logistic regression analysis was used to investigate the association between insulin signaling pathway-related gene polymorphisms and MAFLD in obese children. After adjusting for confounder factors, The Show less
no PDF DOI: 10.11817/j.issn.1672-7347.2023.220295
NR1H3

Contributions of NR1H3 genetic polymorphisms to susceptibility and effects of narrowband UVB phototherapy to nonsegmental vitiligo.

Meifeng Xu, Qiuyu Xu, Yan Liu +5 more · 2023 · Scientific reports · Nature · added 2026-04-24
Vitiligo is the most common depigmenting disorder to which both genetic and environmental factors contribute. The aim of the current work was to evaluate the relationship between polymorphisms of the Show more
Vitiligo is the most common depigmenting disorder to which both genetic and environmental factors contribute. The aim of the current work was to evaluate the relationship between polymorphisms of the gene nuclear receptor subfamily 1 Group H member 3 (NR1H3) and the risk of vitiligo and phototherapy effects in the Chinese Han population. Two independent samples were enrolled to form the discovery set (comprised of 1668 nonsegmental vitiligo [NSV] patients and 2542 controls) and the validation set (comprised of 745 NSV patients and 1492 controls). A total of 13 tag single nucleotide polymorphisms (SNPs) were genotyped in the samples from the discovery stage. SNPs that achieved nominal significance were validated in another independent sample set. The serum level of NR1H3 protein was assayed using enzyme-linked immunosorbent assay kits in the validation set. Genetic association analysis was carried out at allelic and genotypic levels. The therapeutic effects of significant SNPs were examined in the validation set. The SNP rs3758672 was significantly associated with NSV. The A allele was correlated with NSV risk and poorer therapeutic effects. The A allele was strongly correlated with the increased level of serum NR1H3 in both controls and patients. In summary, SNP rs3758672 in NR1H3 was significantly associated with both disease susceptibility and individualized therapeutic effects of NSV in study participants with Han Chinese ancestry. Show less
no PDF DOI: 10.1038/s41598-023-30047-7
NR1H3

circFAM134B is a key factor regulating reticulophagy-mediated ferroptosis in hepatocellular carcinoma.

Tao Bi, Qianqian Lu, Xiaohong Pan +6 more · 2023 · Cell cycle (Georgetown, Tex.) · Taylor & Francis · added 2026-04-24
Ferroptosis is an important mode of regulated cell death (RCD). Its inhibition is closely related to therapeutic resistance and poor prognosis in hepatocellular carcinoma (HCC). Previous reports have Show more
Ferroptosis is an important mode of regulated cell death (RCD). Its inhibition is closely related to therapeutic resistance and poor prognosis in hepatocellular carcinoma (HCC). Previous reports have demonstrated ferroptosis as a biological process highly dependent on selective autophagy, such as ferritinophagy, lipophagy, and clockophagy. Our study also revealed a role for ER-phagy-mediated ferroptosis in HCC cells treated with multi-targeted tyrosine kinase inhibitors (TKIs). In the current study, we found that the homologous circular RNA (circRNA) of the family with sequence similarity 134, member B ( Show less
no PDF DOI: 10.1080/15384101.2023.2249302
PABPC4

Identification and validation of novel signature associated with hepatocellular carcinoma prognosis using Single-cell and WGCNA analysis.

Hang Song, Yang Ge, Jing Xu +4 more · 2023 · International journal of medical sciences · added 2026-04-24
no PDF DOI: 10.7150/ijms.79274
PABPC4

PATJ and MPDZ are required for trophectoderm lineage specification in early mouse embryos.

Mingxi Yu, Xinlong Jiang, Wenyang Cai +6 more · 2023 · Reproduction (Cambridge, England) · added 2026-04-24
During the morula to blastocyst transformation, polarity establishment in outer cells is a prerequisite for trophectoderm lineage specification. This study reveals the roles of polarity proteins PATJ Show more
During the morula to blastocyst transformation, polarity establishment in outer cells is a prerequisite for trophectoderm lineage specification. This study reveals the roles of polarity proteins PATJ and MPDZ in trophectoderm lineage fate decision. In mouse preimplantation embryos, cell polarity plays a crucial role in the first lineage specification. PATJ and its homolog MPDZ are the main members of CRB-PALS1-PATJ (CRUMBS-Protein associated with Lin7 1-Pals-associated tight junction protein) apical polarity complex. They act as adaptor proteins connecting CRB-PALS1 and tight junction proteins, making them essential for cell polarization and stabilization of apical junctions. However, their roles in regulating trophectoderm differentiation and blastocyst development remain unclear. In this study, PATJ and/or MPDZ were downregulated by the microinjection of specific RNA interference constructs into zygotes. Downregulation of PATJ alone did not severely affect early embryonic development and trophectoderm lineage differentiation although it slowed down the blastocyst formation. Depletion of PATJ and MPDZ did not affect compaction and morula development but impaired blastocyst formation. Furthermore, the expression of trophectoderm-specific transcription factors and trophoblast differentiation was compromised in the absence of PATJ/MPDZ. These abnormalities might result from the breakdown of apical domain in the outer cells of the embryo. The loss of PATJ/MPDZ caused the breakdown of CRB and PAR polarity complexes as well as deficiencies in tight junctions and actin filaments. These defects led to ectopic activation of Hippo signaling in the outer cells of developing embryos, ultimately suppressing Cdx2 expression and trophectoderm differentiation. Altogether, PATJ and MPDZ are essential for trophectoderm lineage differentiation and normal blastocyst morphogenesis via the regulation of the establishment of apical domain, formation of tight junctions, phosphorylation and localization of YAP, and expression of trophectoderm-specific transcription factors. Show less
no PDF DOI: 10.1530/REP-22-0429
PATJ

CD44 connects autophagy decline and ageing in the vascular endothelium.

Lu Zhang, Peichang Yang, Jingxuan Chen +17 more · 2023 · Nature communications · Nature · added 2026-04-24
The decline of endothelial autophagy is closely related to vascular senescence and disease, although the molecular mechanisms connecting these outcomes in vascular endothelial cells (VECs) remain uncl Show more
The decline of endothelial autophagy is closely related to vascular senescence and disease, although the molecular mechanisms connecting these outcomes in vascular endothelial cells (VECs) remain unclear. Here, we identify a crucial role for CD44, a multifunctional adhesion molecule, in controlling autophagy and ageing in VECs. The CD44 intercellular domain (CD44ICD) negatively regulates autophagy by reducing PIK3R4 and PIK3C3 levels and disrupting STAT3-dependent PtdIns3K complexes. CD44 and its homologue clec-31 are increased in ageing vascular endothelium and Caenorhabditis elegans, respectively, suggesting that an age-dependent increase in CD44 induces autophagy decline and ageing phenotypes. Accordingly, CD44 knockdown ameliorates age-associated phenotypes in VECs. The endothelium-specific CD44ICD knock-in mouse is shorter-lived, with VECs exhibiting obvious premature ageing characteristics associated with decreased basal autophagy. Autophagy activation suppresses the premature ageing of human and mouse VECs overexpressing CD44ICD, function conserved in the CD44 homologue clec-31 in C. elegans. Our work describes a mechanism coordinated by CD44 function bridging autophagy decline and ageing. Show less
no PDF DOI: 10.1038/s41467-023-41346-y
PIK3C3

Acetylation in the regulation of autophagy.

Yinfeng Xu, Wei Wan · 2023 · Autophagy · Taylor & Francis · added 2026-04-24
Post-translational modifications, such as phosphorylation, ubiquitination and acetylation, play crucial roles in the regulation of autophagy. Acetylation has emerged as an important regulatory mechani Show more
Post-translational modifications, such as phosphorylation, ubiquitination and acetylation, play crucial roles in the regulation of autophagy. Acetylation has emerged as an important regulatory mechanism for autophagy. Acetylation regulates autophagy initiation and autophagosome formation by targeting core components of the ULK1 complex, the BECN1-PIK3C3 complex, and the LC3 lipidation system. Recent studies have shown that acetylation occurs on the key proteins participating in autophagic cargo assembly and autophagosome-lysosome fusion, such as SQSTM1/p62 and STX17. In addition, acetylation controls autophagy at the transcriptional level by targeting histones and the transcription factor TFEB. Here, we review the current knowledge on acetylation of autophagy proteins and their regulations and functions in the autophagy pathway with focus on recent findings. Show less
no PDF DOI: 10.1080/15548627.2022.2062112
PIK3C3

WHOLE GENOME SEQUENCING ANALYSIS OF BODY MASS INDEX IDENTIFIES NOVEL AFRICAN ANCESTRY-SPECIFIC RISK ALLELE.

Xinruo Zhang, Jennifer A Brody, Mariaelisa Graff +120 more · 2023 · medRxiv : the preprint server for health sciences · Cold Spring Harbor Laboratory · added 2026-04-24
Xinruo Zhang, Jennifer A Brody, Mariaelisa Graff, Heather M Highland, Nathalie Chami, Hanfei Xu, Zhe Wang, Kendra Ferrier, Geetha Chittoor, Navya S Josyula, Xihao Li, Zilin Li, Matthew A Allison, Diane M Becker, Lawrence F Bielak, Joshua C Bis, Meher Preethi Boorgula, Donald W Bowden, Jai G Broome, Erin J Buth, Christopher S Carlson, Kyong-Mi Chang, Sameer Chavan, Yen-Feng Chiu, Lee-Ming Chuang, Matthew P Conomos, Dawn L DeMeo, Margaret Du, Ravindranath Duggirala, Celeste Eng, Alison E Fohner, Barry I Freedman, Melanie E Garrett, Xiuqing Guo, Chris Haiman, Benjamin D Heavner, Bertha Hidalgo, James E Hixson, Yuk-Lam Ho, Brian D Hobbs, Donglei Hu, Qin Hui, Chii-Min Hwu, Rebecca D Jackson, Deepti Jain, Rita R Kalyani, Sharon L R Kardia, Tanika N Kelly, Ethan M Lange, Michael LeNoir, Changwei Li, Loic Le Marchand, Merry-Lynn N McDonald, Caitlin P McHugh, Alanna C Morrison, Take Naseri, NHLBI Trans-Omics for Precision Medicine (TOPMed) Consortium, Jeffrey O'Connell, Christopher J O'Donnell, Nicholette D Palmer, James S Pankow, James A Perry, Ulrike Peters, Michael H Preuss, D C Rao, Elizabeth A Regan, Sefuiva M Reupena, Dan M Roden, Jose Rodriguez-Santana, Colleen M Sitlani, Jennifer A Smith, Hemant K Tiwari, Ramachandran S Vasan, Zeyuan Wang, Daniel E Weeks, Jennifer Wessel, Kerri L Wiggins, Lynne R Wilkens, Peter W F Wilson, Lisa R Yanek, Zachary T Yoneda, Wei Zhao, Sebastian Zöllner, Donna K Arnett, Allison E Ashley-Koch, Kathleen C Barnes, John Blangero, Eric Boerwinkle, Esteban G Burchard, April P Carson, Daniel I Chasman, Yii-der Ida Chen, Joanne E Curran, Myriam Fornage, Victor R Gordeuk, Jiang He, Susan R Heckbert, Lifang Hou, Marguerite R Irvin, Charles Kooperberg, Ryan L Minster, Braxton D Mitchell, Mehdi Nouraie, Bruce M Psaty, Laura M Raffield, Alexander P Reiner, Stephen S Rich, Jerome I Rotter, M Benjamin Shoemaker, Nicholas L Smith, Kent D Taylor, Marilyn J Telen, Scott T Weiss, Yingze Zhang, Nancy Heard-Costa, Yan V Sun, Xihong Lin, L Adrienne Cupples, Leslie A Lange, Ching-Ti Liu, Ruth J F Loos, Kari E North, Anne E Justice Show less
Obesity is a major public health crisis associated with high mortality rates. Previous genome-wide association studies (GWAS) investigating body mass index (BMI) have largely relied on imputed data fr Show more
Obesity is a major public health crisis associated with high mortality rates. Previous genome-wide association studies (GWAS) investigating body mass index (BMI) have largely relied on imputed data from European individuals. This study leveraged whole-genome sequencing (WGS) data from 88,873 participants from the Trans-Omics for Precision Medicine (TOPMed) Program, of which 51% were of non-European population groups. We discovered 18 BMI-associated signals ( Show less
no PDF DOI: 10.1101/2023.08.21.23293271
POC5

Safety and efficacy of atezolizumab in Chinese patients with previously treated locally advanced or metastatic non-small cell lung cancer: An open-label, single-arm, multicenter study.

Yanjun Xu, Zhiyu Huang, Jianhua Chang +10 more · 2023 · Lung cancer (Amsterdam, Netherlands) · Elsevier · added 2026-04-24
To evaluate the long-term safety and efficacy of atezolizumab monotherapy in Chinese patients with previously treated, locally advanced or metastatic non-small cell lung cancer (NSCLC). In this open-l Show more
To evaluate the long-term safety and efficacy of atezolizumab monotherapy in Chinese patients with previously treated, locally advanced or metastatic non-small cell lung cancer (NSCLC). In this open-label, single-arm, multicenter study, patients received atezolizumab 1200 mg intravenously on Day 1 of each 21-day cycle. The primary endpoint was incidence of atezolizumab-related serious adverse events (SAEs). Secondary endpoints included other safety and efficacy measures. Patients with available tumor tissue and blood samples underwent biomarker analyses. Patients with available tumor biopsies underwent exome sequencing. The safety and evaluable populations included 101 and 97 patients, respectively. Exome sequencing data were available for 31 patients. Median follow-up time was 27.43 months. Atezolizumab-related SAEs and immune-related adverse events occurred in 25.7% and 47.5% of the safety population, respectively, and in the following subgroups: central nervous system metastases (n = 14), 35.7% and 35.7%; squamous NSCLC (n = 39), 33.3% and 53.8%. The 24-month overall survival rate was 37.4%. Median overall survival and progression-free survival by RECIST v1.1 were 15.31 and 2.86 months, respectively; objective response rate was 16.5% in the evaluable population. PRRC2C (odds ratio: 12.780, P = 0.014) and ZMYND8 (odds ratio: 19.963, P = 0.016) gene mutations were significantly enriched in atezolizumab responders vs non-responders. Patients with CD8 No new safety concerns were raised, and clinically meaningful benefits of atezolizumab monotherapy were shown. The results of the biomarker analyses may guide future therapeutic strategies. Show less
no PDF DOI: 10.1016/j.lungcan.2023.107288
PRRC2C

Silencing proline-rich coiled-coil 2C inhibit the proliferation and metastasis of liver cancer cells.

Kai Zhang, Jiaming Xu, Ran Chen · 2023 · Journal of gastrointestinal oncology · added 2026-04-24
Proline-rich coiled-coil 2C ( The Cancer Genome Atlas (TCGA) RNA-sequencing datasets of 371 cases of primary liver cancer and 50 normal liver tissue specimens were obtained to analyze correlation betw Show more
Proline-rich coiled-coil 2C ( The Cancer Genome Atlas (TCGA) RNA-sequencing datasets of 371 cases of primary liver cancer and 50 normal liver tissue specimens were obtained to analyze correlation between Analysis of TCGA data sets revealed that patients with high Show less
no PDF DOI: 10.21037/jgo-23-10
PRRC2C

Liraglutide intervention improves high-glucose-induced reactive gliosis of Müller cells and ECM dysregulation.

Yongyan Shan, Xinyuan Gao, Kangqi Zhao +8 more · 2023 · Molecular and cellular endocrinology · Elsevier · added 2026-04-24
Reactive gliosis of Müller cells plays an important role in the pathogenesis of diabetic retinopathy (DR). Liraglutide, a glucagon-like peptide-1 receptor (GLP-1R) agonist, has been shown to improve D Show more
Reactive gliosis of Müller cells plays an important role in the pathogenesis of diabetic retinopathy (DR). Liraglutide, a glucagon-like peptide-1 receptor (GLP-1R) agonist, has been shown to improve DR by inhibiting reactive gliosis. However, the mechanism of inhibition has yet to be elucidated. This study investigated the effects of liraglutide on Müller glia reactivity in the early stages of DR and the underlying mechanisms. Proteomics combined with bioinformatics analysis, HE staining, and immunofluorescence staining revealed ganglion cell loss, reactive gliosis of Müller cells, and extracellular matrix (ECM) imbalance in rats with early stages of DR. High glucose (HG) exposure up-regulated GFAP and TNF-α expression and down-regulated ITGB1 expression and FN1 content in extracellular fluid in rMC1 cells, thereby promoting reactive gliosis. GLP-1R knockdown and HG+DAPT inhibition experiments show that liraglutide balances ECM levels by inhibiting activation of the Notch1/Hes1 pathway and ameliorates high-glucose-induced Müller glia reactivity. Thus, the study provides new targets and ideas for improvement of DR in early stages. Show less
no PDF DOI: 10.1016/j.mce.2023.112013
RMC1

Aquaporin 11 alleviates retinal Müller intracellular edema through water efflux in diabetic retinopathy.

Chaoyang Zhang, Dawei Luo, Hai Xie +10 more · 2023 · Pharmacological research · Elsevier · added 2026-04-24
Retinal Müller glial dysfunction and intracellular edema are important mechanisms leading to diabetic macular edema (DME). Aquaporin 11 (AQP11) is primarily expressed in Müller glia with unclear funct Show more
Retinal Müller glial dysfunction and intracellular edema are important mechanisms leading to diabetic macular edema (DME). Aquaporin 11 (AQP11) is primarily expressed in Müller glia with unclear functions. This study aims to explore the role of AQP11 in the pathogenesis of intracellular edema of Müller glia in diabetic retinopathy (DR). Here, we found that AQP11 expression, primarily located at the endfeet of Müller glia, was down-regulated with diabetes progression, accompanied by intracellular edema, which was alleviated by intravitreal injection of lentivirus-mediated AQP11 overexpression. Similarly, intracellular edema of hypoxia-treated rat Müller cell line (rMC-1) was aggravated by AQP11 inhibition, while attenuated by AQP11 overexpression, accompanied by enhanced function in glutamate metabolism and reduced cell death. The down-regulation of AQP11 was also verified in the Müller glia from the epiretinal membranes (ERMs) of proliferative DR (PDR) patients. Mechanistically, down-regulation of AQP11 in DR was mediated by the HIF-1α-dependent and independent miRNA-AQP11 axis. Overall, we deciphered the AQP11 down-regulation, mediated by miRNA-AQP11 axis, resulted in Müller drainage dysfunction and subsequent intracellular edema in DR, which was partially reversed by AQP11 overexpression. Our findings propose a novel mechanism for the pathogenesis of DME, thus targeting AQP11 regulation provides a new therapeutic strategy for DME. Show less
no PDF DOI: 10.1016/j.phrs.2022.106559
RMC1

Genome-Wide Association Study of Body Conformation Traits in a Three-Way Crossbred Commercial Pig Population.

Shaoxiong Deng, Yibin Qiu, Zhanwei Zhuang +10 more · 2023 · Animals : an open access journal from MDPI · MDPI · added 2026-04-24
Body conformation is the most direct production index, which can fully reflect pig growth status and is closely related to critical economic traits. In this study, we conducted a genome-wide associati Show more
Body conformation is the most direct production index, which can fully reflect pig growth status and is closely related to critical economic traits. In this study, we conducted a genome-wide association study (GWAS) on body conformation traits in a population of 1518 Duroc × (Landrace × Yorkshire) commercial pigs. These traits included body length (BL), body height (BH), chest circumference (CC), abdominal circumference (AC), and waist circumference (WC). Both the mixed linear model (MLM) and fixed and random model circulating probability unification (FarmCPU) approaches were employed for the analysis. Our findings revealed 60 significant single nucleotide polymorphisms (SNPs) associated with these body conformation traits in the crossbred pig population. Specifically, sixteen SNPs were significantly associated with BL, three SNPs with BH, thirteen SNPs with CC, twelve SNPs with AC, and sixteen SNPs with WC. Moreover, we identified several promising candidate genes located within the genomic regions associated with body conformation traits. These candidate genes include Show less
no PDF DOI: 10.3390/ani13152414
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MiR-21 Participates in Anti-VEGF-Induced Epithelial Mesenchymal Transformation in RPE Cells.

Xianghui Hao, Yingbin Hua, Chaohui Xie +1 more · 2023 · Clinical ophthalmology (Auckland, N.Z.) · added 2026-04-24
To explore the role and possible mechanism of ARPE-19 cells were exposed to clinical dosage of bevacizumab and Clinical dosage of bevacizumab caused EMT and enhanced
no PDF DOI: 10.2147/OPTH.S427894
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TPPP3 promote epithelial-mesenchymal transition via Snail1 in glioblastoma.

Xu Xu, Yunan Hou, Niya Long +9 more · 2023 · Scientific reports · Nature · added 2026-04-24
Tubulin polymerization promoting protein 3 (TPPP3), a member of the tubulin polymerization family, participates in cell progressions in several human cancers, its biological function and the underlyin Show more
Tubulin polymerization promoting protein 3 (TPPP3), a member of the tubulin polymerization family, participates in cell progressions in several human cancers, its biological function and the underlying mechanisms in glioblastoma multiforme (GBM) remain unclear. Here, we investigated the role and application value of TPPP3 in gliomas and found that the expression of TPPP3 in glioma was higher than that in normal brain tissue (NBT), and increased with the grade of glioma. Up-regulation of TPPP3 expression in glioblastoma cells confer stronger ability of migration, invasion, proliferation and lower apoptosis in vitro. Inhibition of TPPP3 expression in GBM could reduce the migration, invasion, proliferation and induce the apoptosis of glioblastoma cells. TPPP3 affected the process of EMT by regulating the expression of Snail 1 protein. In clinical data analysis, we found a positive correlation between TPPP3 and Snail1 protein expression levels in glioblastomas. Low TPPP3 expression leads to better survival expectations in glioblastomas patients. The content of this study paves the way for further in-depth exploration of the role of TPPP3 in glioblastoma in the future, and provides new treatment and research directions. Show less
no PDF DOI: 10.1038/s41598-023-45233-w
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