👤 Riping Wu

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Also published as: Jiake Wu, Ming-Jiuan Wu, Siying Wu, Yijian Wu, Fong-Li Wu, Chih-Chung Wu, Jin'en Wu, Zixiang Wu, D P Wu, Zhongwei Wu, Haiping Wu, Geyan Wu, Qi-Zhu Wu, Jianjin Wu, Shwu-Yuan Wu, Su Wu, Xiaodi Wu, Changxin Wu, Kuen-Phon Wu, Zhiping Wu, Guofeng Wu, Xiaojun Wu, Qibing Wu, Cheng-Hsin Wu, Junhua Wu, Xiaoting Wu, Wenze Wu, Hong Wu, Yandi Wu, Zhong Wu, An-Chih Wu, Jianhui Wu, Xiaoke Wu, Zhenguo Wu, Jason H Y Wu, Yi-Mi Wu, Bing-Bing Wu, Selena Meiyun Wu, M Wu, Hui-Mei Wu, Danni Wu, Minqing Wu, Sijie Wu, Geng-ze Wu, Kun Wu, Cheng-Hua Wu, Shaofei Wu, Zhaoyang Wu, Qihan Wu, Kunling Wu, R Ryanne Wu, Hao Wu, Mingxuan Wu, Pei Wu, Wendy Wu, Yukang Wu, Douglas C Wu, Jingtao Wu, Guizhen Wu, Zhangjie Wu, Lili Wu, Jianwu Wu, Min-Jiao Wu, Biaoliang Wu, Huan Wu, Shengxi Wu, Fei-Fei Wu, Peih-Shan Wu, Guoqing Wu, Yu-Yuan Wu, Pei-Yu Wu, Lun-Gang Wu, Jing Wu, Geting Wu, Dongzhe Wu, G Wu, Junlong Wu, Jia-Jun Wu, Jiangyue Wu, Muzhou Wu, Ray-Chin Wu, Junzhu Wu, Jian-Qiu Wu, T Wu, Jianxiong Wu, Liping Wu, Haiwei Wu, Yong-Hao Wu, Guoping Wu, Jin-hua Wu, Yi Wu, Chongming Wu, You Wu, Xudong Wu, Qunzheng Wu, Liqiang Wu, Cuiling Wu, Kunfang Wu, Bian Wu, Limeng Wu, Jason Wu, Zhibing Wu, Shuying Wu, Naqiong Wu, Caihong Wu, Joseph C Wu, Huating Wu, Tianhao Wu, Zhi-Hong Wu, Congying Wu, Gaojun Wu, Chiao-En Wu, Dongping Wu, Li Wu, Haixia Wu, Yihang Wu, Shaoxuan Wu, Gen Wu, Fanchang Wu, Xiaorong Wu, Mingjie Wu, Mei Wu, Jiahao Wu, Jiapei Wu, Lingqian Wu, Jia Wu, Fangge Wu, Sen-Chao Wu, Yanhui Wu, Zhiqiang Wu, Sarah Wu, Shugeng Wu, Dongmei Wu, Xuanqin Wu, Caiwen Wu, Junjing Wu, Jiangdong Wu, Guihua Wu, Yingbiao Wu, Meini Wu, Rui Wu, Hua-Yu Wu, Bifeng Wu, Jingwan Wu, Lingling Wu, Junzheng Wu, Xinmiao Wu, Yi-Fang Wu, Yuyi Wu, Qinglin Wu, Yixuan Wu, Leilei Wu, Bin Wu, Tianqi Wu, Shiya Wu, Hui-Chen Wu, Jian Wu, Sijun Wu, Yiwen Wu, Cong Wu, Feng Wu, Xi-Ze Wu, Qiuji Wu, Alexander T H Wu, Semon Wu, Qinan Wu, Lai Man Natalie Wu, Zhuokai Wu, Ran Wu, Panyun Wu, Kui Wu, Yumei Wu, Xinrui Wu, Biwei Wu, Yueling Wu, Xing Wu, Jiayi Wu, Hua Wu, Yuen-Jung Wu, Bingjie Wu, Xiaoliang Wu, Matthew A Wu, Jin Wu, Juanjuan Wu, Qiuhong Wu, Xiaoming Wu, Hongfu Wu, Ming-Sian Wu, Ronghua Wu, Junduo Wu, Dandan Wu, Ming-Shiang Wu, Yuliang Wu, Ying-Ying Wu, Chaoling Wu, Guang-Liang Wu, De Wu, Yihua Wu, Yuanyuan Wu, Tsung-Jui Wu, Han Wu, Yulian Wu, Lipeng Wu, Zhihao Wu, Jiexi Wu, Anna H Wu, Huazhen Wu, Qiu Wu, Yaqin Wu, Shengru Wu, Chieh-Lin Stanley Wu, Xiaoqian Wu, Xiahui Wu, Yun-Wen Wu, Jian-Yi Wu, Jianli Wu, Qiuya Wu, Tsai-Kun Wu, Xinyin Wu, Guoyao Wu, Zhenfeng Wu, Guoli Wu, J W Wu, Bill X Wu, Zujun Wu, Jianliang Wu, Yuanshun Wu, Ling-Ying Wu, Zeng-An Wu, Jianrong Wu, Xue Wu, Ke Wu, Mengxue Wu, Cheng-Yang Wu, Jinghong Wu, Rongrong Wu, Ruolan Wu, Rong Wu, Kevin Zl Wu, Xiaohong Wu, Run Wu, Zaihao Wu, Yu-Ke Wu, Chaowei Wu, Anyue Wu, Xinjing Wu, Yun Wu, Xuan Wu, Meili Wu, Shu Wu, Wanxia Wu, Yi-No Wu, Chao-Liang Wu, Chengwei Wu, Y-W Wu, Pensee Wu, Zhao-Bo Wu, Guangxian Wu, Xiao Wu, Juanli Wu, Xinlei Wu, Changjie Wu, Sai Wu, Yujuan Wu, Jiawei Wu, Haoze Wu, Renlv Wu, Xiaoyang Wu, Yipeng Wu, Yuh-Lin Wu, Yu'e Wu, An-Hua Wu, Dan-Chun Wu, Meng-Chao Wu, Yuanhao Wu, Jer-Yuarn Wu, Qian-Yan Wu, Guangyan Wu, Huisheng Wu, Huijuan Wu, Shuting Wu, Long-Jun Wu, Alice Ying-Jung Wu, Xiru Wu, Zhenfang Wu, Lidi Wu, Yetong Wu, Disheng Wu, Linmei Wu, Huiwen Wu, Zhenzhou Wu, Yuhong Wu, Liang Wu, Liyan Wu, Kuan-Li Wu, Pei-Ting Wu, Xiao-Jin Wu, Terence Wu, Lifeng Wu, Shujuan Wu, Gang Wu, Xue-Mei Wu, Szu-Hsien Wu, Yan-ling Wu, Xiaokang Wu, Lingyan Wu, Yih-Jer Wu, Xinghua Wu, Chunfu Wu, Yingxia Wu, Rongling Wu, Xifeng Wu, Jinhua Wu, Sihan Wu, Ming-Yue Wu, Shiyang Wu, K D Wu, Jinmei Wu, Luyan Wu, Shin-Long Wu, Shuai Wu, Zhipeng Wu, Guangzhen Wu, Zhixiang Wu, Longting Wu, Zhengsheng Wu, Xiaoqiong Wu, Yaoxing Wu, Yuqin Wu, Yudan Wu, Hongting Wu, Zoe Wu, Chi-Jen Wu, R Wu, Meina Wu, Zhongqiu Wu, Dengying Wu, Anke Wu, Cheng-Jang Wu, Hsi-Chin Wu, Shufang Wu, Yongjiang Wu, Yuan-de Wu, Sihui Wu, Qi Wu, Wenhui Wu, Fenfang Wu, K S Wu, Jianzhi Wu, Nana Wu, Lin-Han Wu, Jinjun Wu, Zhen Wu, Chen-Lu Wu, Jing-Fang Wu, Haiyan Wu, Yihui Wu, Qiqing Wu, Zhengzhi Wu, Dai-Chao Wu, Zhenyan Wu, Wen-Jeng Wu, Guanming Wu, Yongqun Wu, Sean M Wu, Hei-Man Wu, Su-Hui Wu, Diana H Wu, Ben J Wu, Pingxian Wu, Chew-Wun Wu, Yillin Wu, Xiaobing Wu, Jiang-Bo Wu, Jerry Wu, Siming Wu, Zijun Wu, Daqing Wu, Yu-Hsuan Wu, Lichao Wu, Zhimin Wu, Daxian Wu, Qijing Wu, Zhaoyi Wu, Z Wu, Tong Wu, Cheng-Chun Wu, Tracy Wu, Shusheng Wu, D Wu, Ting-Ting Wu, Xiao-Yan Wu, J Wu, Lan Wu, Changchen Wu, Qi-Fang Wu, Changwei Wu, Liangyan Wu, Liufeng Wu, Kan Wu, Eugenia Wu, Mingming Wu, Xiaolong Wu, Chunru Wu, Zhaofei Wu, Shenhao Wu, Li-Peng Wu, Yuna Wu, Minna Wu, Justin Che-Yuen Wu, Buling Wu, Wutian Wu, Chengyu Wu, Yuwei Wu, Guixin Wu, Hei Man Wu, Haijing Wu, Qiuchen Wu, Xiao-Hui Wu, Junfei Wu, Wenda Wu, Xiaofeng Wu, Linyu Wu, Yung-Fu Wu, Mengbo Wu, Zhenling Wu, Zuping Wu, Maoqing Wu, Chun-Chieh Wu, Julian Wu, Binbin Wu, Xiaohui Wu, Qian Wu, Xinchun Wu, Shuisheng Wu, Linxiang Wu, Xueqing Wu, Bo Wu, Moxin Wu, Xiao-Cheng Wu, Anzhou Wu, Shuyi Wu, Jiahui Wu, Meiqin Wu, Shihao Wu, Jer-Yuan Wu, Wen-Shu Wu, Wudelehu Wu, Ruonan Wu, Song Wu, De-Fu Wu, Yulin Wu, Hongyu Wu, Yurong Wu, Zixuan Wu, Shih-Ying Wu, Chih-Hsing Wu, Chengrong Wu, Yinghao Wu, Yuanzhao Wu, Baochuan Wu, Wenjie Wu, Ziliang Wu, Liuting Wu, Chia-Ling Wu, Y Q Wu, Man Wu, Na Wu, Wutain Wu, Chenyang Wu, Jinyu Wu, Selwin K Wu, Ping Wu, Lorna Wu, D I Wu, Yi-Cheng Wu, Jianzhong Wu, Xiaoyun Wu, Zhourui Wu, Li-Jun Wu, Xinhe Wu, Zhi-Wei Wu, Yinan Wu, Xinyan Wu, Xin Wu, Ting-Feng Wu, Yawei Wu, Shixin Wu, Hong-Mei Wu, Xiaojin Wu, Tsung-Teh Wu, Jiarui Wu, Yiqun Wu, Qi-Nian Wu, Ju Wu, Kai-Yue Wu, Xi-Chen Wu, Pengjie Wu, Zhe Wu, Shaoping Wu, Zhou Wu, Han-Jie Wu, Haijiang Wu, Weijie Wu, Xiaojie Wu, Hongfei Wu, Yi-Ying Wu, Zhentian Wu, Ze Wu, Kai-Hong Wu, Yuting Wu, Minyao Wu, Xueyan Wu, Shinan Wu, Feifei Wu, Yonghui Wu, Haoxuan Wu, Yanzhi Wu, Yiyi Wu, Dong Wu, Guohao Wu, Wenjing Wu, Shibo Wu, Wenqian Wu, Tian Wu, Tiantian Wu, Hai-Yan Wu, Chong Wu, Hongxian Wu, Daoyuan Wu, Zongfu Wu, Ling Wu, Yuxiang Wu, Xilong Wu, Yuyu Wu, Huijian Wu, Fengming Wu, Zong-Jia Wu, Guorong Wu, Chuanhong Wu, Choufei Wu, Chi-Chung Wu, Junfang Wu, Xingwei Wu, Ling-Fei Wu, Xiaoqing Wu, Xinyang Wu, Xiaomin Wu, Yili Wu, Hong-Fu Wu, Shao-Ming Wu, Thomas D Wu, Lizhen Wu, Yuanming Wu, Hsien-Ming Wu, Jian Hui Wu, Litong Wu, Yuxian Wu, Weihua Wu, Lei Wu, C Wu, Wei Wu, Yu-E Wu, Qiulian Wu, Mei-Hwan Wu, Yuexiu Wu, Shaoze Wu, Zilong Wu, Chi-Hao Wu, Baojin Wu, Chao Wu, Yao Wu, Ya Wu, Do-Bo Wu, Wenjun Wu, Zhongren Wu, Nini Wu, Michael C Wu, Ning Wu, Jie Wu, Ming J Wu, Yi-Syuan Wu, Limei Wu, Zhenzhen Wu, Tianwen Wu, Wen-Chieh Wu, Junfeng Wu, Yunhua Wu, Shunan Wu, Junqi Wu, Jianing Wu, Honglin Wu, Maureen Wu, Yexiang Wu, Yan-Hua Wu, Mengjun Wu, Y H Wu, Mingxing Wu, Liuying Wu, Suhua Wu, Xiaomeng Wu, Shyh-Jong Wu, Tung-Ho Wu, Hongliang Wu, Wenxian Wu, Xuekun Wu, Ed Xuekui Wu, Wenqiang Wu, Chuang Wu, Jingyi Wu, Duojiao Wu, Xueyuan Wu, Ji-Zhou Wu, Lianqian Wu, Gaige Wu, Qing-Qian Wu, Haihu Wu, Xiushan Wu, Xueyao Wu, Tingchun Wu, Yafei Wu, Lingxi Wu, R-J Wu, Weidong Wu, Re-Wen Wu, Zhidan Wu, Peiyao Wu, Xuemei Wu, Chen Wu, Yiting Wu, Kerui Wu, Lihong Wu, Shiqi Wu, Liren Wu, Xiuhua Wu, Beili Wu, Yongqi Wu, Ruihong Wu, Huini Wu, Guang-Long Wu, Lingyun Wu, Po-Chang Wu, Wenxue Wu, Qinghua Wu, Ru-Zi Wu, Changjing Wu, Wenlin Wu, Xiexing Wu, J Y Wu, Jianping Wu, Guanggeng Wu, W J Wu, Zhichong Wu, Di Wu, Shaoyu Wu, Xiaotong Wu, Junyong Wu, Hui Wu, Hongyan Wu, Shengde Wu, Mengyuan Wu, Yutong Wu, Zheming Wu, Yiping Wu, Wen-Hui Wu, Dapeng Wu, Guiping Wu, Bing Wu, Wen-Sheng Wu, Yunpeng Wu, Li-Ling Wu, Xiao-Yuan Wu, Baiyan Wu, Qiu-Li Wu, Ying Wu, Xiao-Ye Wu, Da-Hua Wu, Hsing-Chieh Wu, Hui-Xuan Wu, Chieh-Jen Wu, Pengning Wu, Sichen Wu, Mengying Wu, S F Wu, Ming-Der Wu, Jia-En Wu, Qi-Jun Wu, Guo-Chao Wu, Weida Wu, Zhenyong Wu, Qi-Biao Wu, Yangfeng Wu, Lijie Wu, Zhiye Wu, Jihui Wu, JieQian Wu, Qianqian Wu, Zhengliang L Wu, Jingyun Wu, Xiaoman Wu, Ruohao Wu, Yiyang Wu, Zhengfeng Wu, Xiao-Jun Wu, Lizi Wu, Qiang Wu, J-Z Wu, Guangjie Wu, Pengfei Wu, Jundong Wu, Jianying Wu, Meng-Ling Wu, Beier Wu, Lingxiang Wu, Jamie L Y Wu, Xilin Wu, Keija Wu, An-Li Wu, Yanhua Wu, Yi-Ming Wu, Chengbiao Wu, Huanghui Wu, Dong-Feng Wu, Kunsheng Wu, Zhengcan Wu, Yuxin Wu, Kun-Rong Wu, Guanxian Wu, Dong-Fang Wu, Sensen Wu, Guifen Wu, Yifeng Wu, Pin Wu, Tzu-Chun Wu, Qingping Wu, R M Wu, Mian Wu, S J Wu, Haisu Wu, Senquan Wu, Jingjing Wu, Cheng Wu, Meng Wu, Geping Wu, Yu Wu, Yumin Wu, Xia Wu, William Ka Kei Wu, Xian-Run Wu, Juan Wu, Pei-Ei Wu, Meng-Hsun Wu, Yingying Wu, S M Wu, Xiangwei Wu, Guangrun Wu, Liuxin Wu, Yangyu Wu, Jia-Hui Wu, Jin-Zhen Wu, Shaohuan Wu, S L Wu, Yanli Wu, June K Wu, Haishan Wu, H Wu, Zhou-Ming Wu, Deqing Wu, Tao Wu, Dong-Bo Wu, Binxin Wu, Yalan Wu, Xiangxin Wu, Xueji Wu, Hongxi Wu, Zhonghui Wu, Jiaxi Wu, Tianzhi Wu, Meiqi Wu, Weiwei Wu, Yan-Jun Wu, Lijuan Wu, Tingqin Wu, Jianming Wu, P L Wu, Yih-Ru Wu, Lanlan Wu, Jianjun Wu, An-Xin Wu, Jianguang Wu, Xingjie Wu, Jianzhang Wu, Xianan Wu, Wei-Ping Wu, Haoan Wu, Fang-Tzu Wu, Wenwen Wu, Zhongjun Wu, Xi Wu, Teng Wu, Xiaoling Wu, Mengjuan Wu, Wen Wu, Yifan Wu, Yang Wu, Qianhu Wu, Shenyue Wu, Wu-Tian Wu, Qianwen Wu, Ye Wu, Lixing Wu, Gui-Qin Wu, Grace F Wu, Xing-Ping Wu, Ming Wu, Lisha Wu, Yanchuan Wu, Yuming Wu, Siqi Wu, Yuan Wu, Yu-Ting Wu, I H Wu, Minghua Wu, Hailong Wu, Zhenlong Wu, B Wu, Fang Wu, Guanzhong Wu, Liqun Wu, Guifu Wu, Chris Y Wu, Zhikang Wu, Qi-Yong Wu, Qingshi Wu, Zhao-Yang Wu, Chih-Ching Wu, Man-Jing Wu, Jun Wu, Jinhui Wu, Jincheng Wu, Linhong Wu, Hung-Tsung Wu, Tangchun Wu, Xinglong Wu, Zhen-Yang Wu, Ma Wu, Dongyan Wu, Yin Wu, Jiu-Lin Wu, Yong Wu, Yan Wu, Weizhen Wu, Changyu Wu, Fanggeng Wu, Dishan Wu, Yi-Long Wu, Yue Wu, Ge-ru Wu, Jinqiao Wu, Jing-Wen Wu, Zhongyang Wu, Lifang Wu, Sheng-Li Wu, Songfen Wu, Jia-Wei Wu, Yihan Wu, Kebang Wu, Wenyong Wu, Cai-Qin Wu, Yilong Wu, Yanan Wu, Hsiu-Chuan Wu, Xueqian Wu, Yen-Wen Wu, Paul W Wu, Xing-De Wu, Ying-Ting Wu, Mingfu Wu, Yucan Wu, Na-Qiong Wu, Linzhi Wu, Jinze Wu, Xuhan Wu, H J Wu, Ruize Wu, Dirong Wu, Chung-Yi Wu, Yaohong Wu, Jianyi Wu, Jugang Wu, Jiao Wu, Liang-Huan Wu, Xueling Wu, Ruying Wu, Gen Sheng Wu, Zhaoyuan Wu, Andong Wu, Shiwen Wu, Hsan-Au Wu, Yu-Ling Wu, Jia-Qi Wu, Xihai Wu, Yanting Wu, Lulu Wu, Xuxian Wu, Xiaomei Wu, Jingyue Wu, Shuihua Wu, Ren Wu, S Wu, Yupeng Wu, Haoming Wu, Samuel M Wu, Fan Wu, Yuesheng Wu, Yihe Wu, Tiange Wu, Shuang Wu, Jiayu Wu, Chia-Lung Wu, Shengnan Wu, Yaojiong Wu, Y Wu, Zhuoze Wu, Y Y Wu, Zimu Wu, Depei Wu, Yi-Hua Wu, Haiyun Wu, Yanyan Wu, Min Wu, Wenjuan Wu, Jinfeng Wu, Guangxi Wu, Junjie Wu, Yawen Wu, Pinglian Wu, Hui-Hui Wu, Xunwei Wu, Xuefeng Wu, Constance Wu, Depeng Wu, Dianqing Wu, Qibiao Wu, Nan Wu, Hao-Tian Wu, Hanyu Wu, Xiaojiang Wu, Cheng-Jun Wu, San-pin Wu, Xiaofan Wu, Xiwei Wu, Shi-Xin Wu, Shao-Guo Wu, Sunyi Wu, Yueheng Wu, Chengqian Wu, Kuixian Wu, Xin-Xi Wu, Guanyi Wu, Qiuxia Wu, Danhong Wu, He Wu, Zhong-Jun Wu, Siyi Wu, Xiangsheng Wu, Lanxiang Wu, Liting Wu, Kaili Wu, Ping-Hsun Wu, Zheng Wu, Wen-Ling Wu, Jiang-Nan Wu, Huanlin Wu, Yongfei Wu, Catherine A Wu, Leslie Wu, Shuo Wu, Peng-Fei Wu, Cho-Kai Wu, Meng-Han Wu, Hon-Yen Wu, Anguo Wu, Yuguang Philip Wu, Hai-Yin Wu, Yicheng Wu, Xiaolang Wu, Yujie Wu, Qing Wu, Haomin Wu, V C Wu, Xingdong Wu, Hengyu Wu, Jiang Wu, Chengxi Wu, Xiaoli Wu, Junyi Wu, Ling-qian Wu, William K K Wu, Chun Wu, Lesley Wu, Niting Wu, Jiayuan Wu, Xueying Wu, Yingning Wu, S-F Wu, David Wu, Joshua L Wu, Mei-Na Wu, Jin-Shang Wu, Guanzhao Wu, Jianqiang Wu, Runda Wu, Li-Hsien Wu, Rongjie Wu, June-Hsieh Wu, Huazhang Wu, Huanwen Wu, Xiu-Zhi Wu, Yanran Wu, Xianfeng Wu, Weibin Wu, Xuanshuang Wu, G X Wu, Yan Yan Wu, Jiaqi Wu, Runpei Wu, Chien-Ting Wu, Li-Na Wu, Qinfeng Wu, Chia-Chang Wu, Yueming Wu, Renhai Wu, Siyu Wu, Baojian Wu, Yi-Xia Wu, Wei-Yin Wu, Renrong Wu, C-H Wu, Chuan-Ling Wu, Xinran Wu, Fengying Wu, Qiuliang Wu, Guanhui Wu, Jinjie Wu, Wei-Chi Wu, Wei-Xun Wu, Meng-Na Wu, Lin Wu, Wan-Fu Wu, Jiajing Wu, Colin Chih-Chien Wu, Yajie Wu, Qiaowei Wu, Yaru Wu, Xiaoping Wu, Xue-Yan Wu, Mengchao Wu, Weijun Wu, Boquan Wu, Zelai Wu, Chunyan Wu, Pei-Wen Wu, Guojun Wu, Yichen Wu, Ming-Tao Wu, Hsueh-Erh Wu, Guang-Bo Wu, Chia-Zhen Wu, Zhi-Yong Wu, Kay L H Wu, Yong-Hong Wu, Anping Wu, Jiahang Wu, Xiaobin Wu, Ching-Yi Wu, Linzhen Wu, Xiaoxing Wu, Haidong Wu, Zhen-Qi Wu, Mark N Wu, Jianmin Wu, Guanrong Wu, Xianpei Wu, An-Dong Wu, Yanchun Wu, Dongsheng Wu, Ren-Chin Wu, Yuchen Wu, Mengna Wu, Lijun Wu, Zhuanbin Wu, Yanjing Wu, Haodi Wu, Lun Wu, Si-Jia Wu, Yongfa Wu, Ximei Wu, Hai-Ping Wu, Wenyu Wu, Xiangping Wu, L-F Wu, Yixia Wu, Haiying Wu, Yiran Wu, Yanhong Wu, Xiayin Wu, Yushun Wu, Yali Wu, Qitian Wu, Qin Wu, Xiaofu Wu, Jiamei Wu, Xiaoyong Wu, Qiong Wu, Xiaoying Wu, Wujun Wu, N Wu, Peiyi Wu, Yongmei Wu, Xiaojing Wu, Yizhou Wu, Dan Wu, Wen-Qiang Wu, Anshi Wu, Junqing Wu, Xiao-Yang Wu, Zhaoxia Wu, Liyang Wu, Hongke Wu, Mengqiu Wu, Peng Wu, Haibin Wu, Ding Lan Wu, Yingzhi Wu, Lecheng Wu, Kejia Wu, Anyi Wu, Junshu Wu, Jianxin Wu, Deguang Wu, Jiaxuan Wu, W Wu, Justin C Y Wu, Jiong Wu, Yu-Chih Wu, Qinglan Wu, Xinyi Wu, Diana Wu, Xuefen Wu, Zhongluan Wu, Yanqiong Wu, Shengming Wu, Jian-Lin Wu, Donglin Wu, Daren Wu, Lintao Wu, Xiaodong Wu, Chang-Jiun Wu, Chunshuai Wu, Irene X Y Wu, Yaping Wu, Xiping Wu, Yangna Wu, Zongheng Wu, Chia-Chen Wu, Wenyi Wu, Yansheng Wu, Shaojun Wu, Aimin Wu, Caisheng Wu, Zhongchan Wu, Xu Wu, Fei Wu, Yaohua Wu, Yibo Wu, Qinyi Wu, Zhengyu Wu, Yadi Wu, Hang Wu, L Wu, Mingjun Wu, Yuetong Wu, Wen-Juan Wu, Guangming Wu, Lingzhi Wu, Tingting Wu, Zhong-Yan Wu, Zhuzhu Wu, Yuanbing Wu, Cuiyan Wu, Colin O Wu, Baoqin Wu, Shuyan Wu, Hongmei Wu, Guangsen Wu, Xiaolin Wu, An Guo Wu, Kailang Wu, Chien-Sheng Wu, Chun-Hua Wu, Jemma X Wu, Wenqi Wu, Quanhui Wu, Qing-Wu Wu, Yanxiang Wu, Jiajin Wu, Yuan Kai Wu, Qiao Wu
articles

Glutamine metabolism-related genes and immunotherapy in nonspecific orbital inflammation were validated using bioinformatics and machine learning.

Zixuan Wu, Na Li, Yuan Gao +3 more · 2024 · BMC genomics · BioMed Central · added 2026-04-24
Nonspecific orbital inflammation (NSOI) is an idiopathic, persistent, and proliferative inflammatory condition affecting the orbit, characterized by polymorphous lymphoid infiltration. Its pathogenesi Show more
Nonspecific orbital inflammation (NSOI) is an idiopathic, persistent, and proliferative inflammatory condition affecting the orbit, characterized by polymorphous lymphoid infiltration. Its pathogenesis and progression have been linked to imbalances in tumor metabolic pathways, with glutamine (Gln) metabolism emerging as a critical aspect in cancer. Metabolic reprogramming is known to influence clinical outcomes in various malignancies. However, comprehensive research on glutamine metabolism's significance in NSOI is lacking. This study conducted a bioinformatics analysis to identify and validate potential glutamine-related molecules (GlnMgs) associated with NSOI. The discovery of GlnMgs involved the intersection of differential expression analysis with a set of 42 candidate GlnMgs. The biological functions and pathways of the identified GlnMgs were analyzed using GSEA and GSVA. Lasso regression and SVM-RFE methods identified hub genes and assessed the diagnostic efficacy of fourteen GlnMgs in NSOI. The correlation between hub GlnMgs and clinical characteristics was also examined. The expression levels of the fourteen GlnMgs were validated using datasets GSE58331 and GSE105149. Fourteen GlnMgs related to NSOI were identified, including FTCD, CPS1, CTPS1, NAGS, DDAH2, PHGDH, GGT1, GCLM, GLUD1, ART4, AADAT, ASNSD1, SLC38A1, and GFPT2. Biological function analysis indicated their involvement in responses to extracellular stimulus, mitochondrial matrix, and lipid transport. The diagnostic performance of these GlnMgs in distinguishing NSOI showed promising results. This study successfully identified fourteen GlnMgs associated with NSOI, providing insights into potential novel biomarkers for NSOI and avenues for monitoring disease progression. Show less
📄 PDF DOI: 10.1186/s12864-023-09946-6
CPS1

Endophytic fungus Penicillium steckii DF33 promoted tanshinones biosynthesis in Salvia miltiorrhiza by regulating the expression of CYP450 genes.

Xiaoman Lv, Wenyi Zhang, Siyuan Chu +8 more · 2024 · Gene · Elsevier · added 2026-04-24
Salvia miltiorrhiza, a prominent traditional Chinese medicinal resource, has been extensively employed in the management of cardiovascular and cerebrovascular ailments. Ensuring the consistency of S. Show more
Salvia miltiorrhiza, a prominent traditional Chinese medicinal resource, has been extensively employed in the management of cardiovascular and cerebrovascular ailments. Ensuring the consistency of S. miltiorrhiza raw materials revolves around the imperative task of maintaining stable tanshinones content and composition. An effective approach in this regard involves the utilization of endophytic fungi as inducers. Within this context, our study spotlights an endophytic fungus, Penicillium steckii DF33, isolated from the roots of S. miltiorrhiza. Remarkably, this fungus has demonstrated a significant capacity to boost the biosynthesis and accumulation of tanshinones. The primary objective of this investigation is to elucidate the underlying regulatory mechanism by which DF33 enhances and regulates the biosynthesis and accumulation of tanshinones. This is achieved through its influence on the differential expression of crucial CYP450 genes within the S. miltiorrhiza hairy roots system. The results revealed that the DF33 elicitor not only promotes the growth of hairy roots but also enhances the accumulation of tanshinones. Notably, the content of cryptotanshinone was reached 1.6452 ± 0.0925 mg g Show less
no PDF DOI: 10.1016/j.gene.2023.148094
CPS1

Exploring the biological roles of DHX36, a DNA/RNA G-quadruplex helicase, highlights functions in male infertility: A comprehensive review.

Li Fu, Qiang Wu, Junjiang Fu · 2024 · International journal of biological macromolecules · Elsevier · added 2026-04-24
It is estimated that 15 % of couples at reproductive age worldwide suffer from infertility, approximately 50 % of cases are caused by male factors. Significant progress has been made in the diagnosis Show more
It is estimated that 15 % of couples at reproductive age worldwide suffer from infertility, approximately 50 % of cases are caused by male factors. Significant progress has been made in the diagnosis and treatment of male infertility through assisted reproductive technology and molecular genetics methods. However, there is still inadequate research on the underlying mechanisms of gene regulation in the process of spermatogenesis. Guanine-quadruplexes (G4s) are a class of non-canonical secondary structures of nucleic acid commonly found in genomes and RNAs that play important roles in various biological processes. Interestingly, the DEAH-box helicase 36 (DHX36) displays high specificity for the G4s which can unwind both DNA G4s and RNA G4s enzymatically and is highly expressed in testis, thereby regulating multiple cellular functions including transcription, pre-mRNA splicing, translation, telomere maintenance, genomic stability, and RNA metabolism in development and male infertility. This review provides an overview of the roles of G4s and DHX36 in reproduction and development. We mainly focus on the potential role of DHX36 in male infertility. We also discuss possible future research directions regarding the mechanism of spermatogenesis mediated by DHX36 through G4s in spermatogenesis-related genes and provide new targets for gene therapy of male infertility. Show less
no PDF DOI: 10.1016/j.ijbiomac.2024.131811
DHX36

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

Glioma stem cell-derived exosomes induce the transformation of astrocytes via the miR-3065-5p/DLG2 signaling axis.

Haoran Li, Jianjun Zhu, Xinglei Liu +9 more · 2024 · Glia · Wiley · added 2026-04-24
Tumor-associated astrocytes (TAAs) in the glioblastoma microenvironment play an important role in tumor development and malignant progression initiated by glioma stem cells (GSCs). In the current stud Show more
Tumor-associated astrocytes (TAAs) in the glioblastoma microenvironment play an important role in tumor development and malignant progression initiated by glioma stem cells (GSCs). In the current study, normal human astrocytes (NHAs) were cultured and continuously treated with GSC-derived exosomes (GSC-EXOs) induction to explore the mechanism by which GSCs affect astrocyte remodeling. This study revealed that GSC-EXOs can induce the transformation of NHAs into TAAs, with relatively swollen cell bodies and multiple extended processes. In addition, high proliferation, elevated resistance to temozolomide (TMZ), and increased expression of TAA-related markers (TGF-β, CD44, and tenascin-C) were observed in the TAAs. Furthermore, GSC-derived exosomal miR-3065-5p could be delivered to NHAs, and miR-3065-5p levels increased significantly in TAAs, as verified by miRNA expression profile sequencing and Reverse transcription polymerase chain reaction. Overexpression of miR-3065-5p also enhanced NHA proliferation, elevated resistance to TMZ, and increased the expression levels of TAA-related markers. In addition, both GSC-EXO-induced and miR-3065-5p-overexpressing NHAs promoted tumorigenesis of GSCs in vivo. Discs Large Homolog 2 (DLG2, downregulated in glioblastoma) is a direct downstream target of miR-3065-5p in TAAs, and DLG2 overexpression could partially reverse the transformation of NHAs into TAAs. Collectively, these data demonstrate that GSC-EXOs induce the transformation of NHAs into TAAs via the miR-3065-5p/DLG2 signaling axis and that TAAs can further promote the tumorigenesis of GSCs. Thus, precisely blocking the interactions between astrocytes and GSCs via exosomes may be a novel strategy to inhibit glioblastoma development, but more in-depth mechanistic studies are still needed. Show less
no PDF DOI: 10.1002/glia.24506
DLG2

Exploring the mechanism of berberine treatment for atherosclerosis combined with non-alcoholic fatty liver disease based on bioinformatic and experimental study.

Shushu Wang, Kachun Lu, Liwen Lin +9 more · 2024 · PloS one · PLOS · added 2026-04-24
Atherosclerosis (AS) and Non-alcoholic fatty liver disease (NAFLD) are chronic metabolic disorders with high prevalence and significant health impacts. Both conditions share common pathophysiological Show more
Atherosclerosis (AS) and Non-alcoholic fatty liver disease (NAFLD) are chronic metabolic disorders with high prevalence and significant health impacts. Both conditions share common pathophysiological pathways including abnormal lipid metabolism and inflammation. Berberine (BBR), an isoquinoline alkaloid, is known for its beneficial effects on various metabolic and cardiovascular disorders. This study investigates BBR's impact on AS and NAFLD through bioinformatics analysis and experimental models. This study utilized various bioinformatics methods, including transcriptome analysis, weighted gene co-expression network analysis (WGCNA), machine learning, and molecular docking, to identify key genes and pathways involved in AS and NAFLD. Subsequently an animal model of AS combined with NAFLD was established using ApoE-/- mice fed a high-fat diet. The efficacy and mechanism of action of BBR were verified using methods such as hematoxylin and eosin (HE) staining, Oil Red O staining, and real-time quantitative PCR (RTqPCR). Through transcriptome analysis, WGCNA, and machine learning, this study identified 48 key genes involved in both AS and NAFLD. Function analysis revealed that the implicated genes were significantly involved in pathways like cytokine-cytokine receptor interaction, chemokine signaling, and IL-17 signaling pathway, suggesting their role in inflammation and immune responses. Single cell validation identified six key genes: dual specificity phosphatase 6 (DUSP6), chemokine ligand 3 (CCL3), complement component 5a receptor 1 (C5AR1), formyl peptide receptor 1 (FPR1), myeloid nuclear differentiation antigen (MNDA), and proviral integration site of murine 2(PIM2). Finally, molecular docking and animal experiments showed that BBR significantly reduced lipid deposits and inflammatory markers in liver and aortic tissues. In conclusion, BBR can improve AS combined with NAFLD by regulating genes like MNDA, PIM2, DUSP6, CCL3, C5AR1, and FPR1, with the mechanism related to inflammation control. The findings suggest potential clinical benefits of BBR in reducing the progression of both AS and NAFLD, warranting further investigation. Show less
📄 PDF DOI: 10.1371/journal.pone.0314961
DUSP6

Utility of patient-derived xenografts to evaluate drug sensitivity and select optimal treatments for individual non-small-cell lung cancer patients.

Xiaoqing Wang, Ju Zhu, Lingling Li +5 more · 2024 · Molecular medicine (Cambridge, Mass.) · BioMed Central · added 2026-04-24
Patient-derived xenograft (PDX) is currently considered a preferred preclinical model to evaluate drug sensitivity, explore drug resistance mechanisms, and select individualized treatment regimens. Hi Show more
Patient-derived xenograft (PDX) is currently considered a preferred preclinical model to evaluate drug sensitivity, explore drug resistance mechanisms, and select individualized treatment regimens. Histopathological examination, immunohistochemistry and whole-exome sequencing confirmed similarity between our PDX tumors and primary tumors in terms of morphology and genetic characteristics. The drug reactivity of the PDX tumor was validated in vivo. The mechanisms of acquired resistance to Osimertinib PDX tumors were investigated by WES and WB. We successfully established 13 NSCLC-PDXs derived from 62 patients, including eight adenocarcinomas, four squamous-cell carcinoma, and one large-cell neuroendocrine carcinoma. Histological subtype and clinical stage were significant factors affecting the successful PDXs establishment. The treatment responses to conventional chemotherapy in PDXs were entirely consistent with that of their corresponding patients. According to the genetic status of tumors, more appropriate targeted agents were selected in PDXs for their corresponding patients as alternative treatment options. In addition, a PDX model with acquired resistance to osimertinib was induced, and the overactivation of RAS mitogen-activated protein kinase (MAPK)-extracellular signal-regulated kinase (ERK) signaling pathway caused by the dual-specificity phosphatase 6 (DUSP6) M62I mutation was found to play a key role in the development of osimertinib resistance. Trametinib, a specific inhibitor of the MAPK-ERK pathway significantly slowed down the tumor growth in osimertinib-resistant PDX models, providing an alternative treatment in patients after osimertinib failure. Show less
📄 PDF DOI: 10.1186/s10020-024-00934-4
DUSP6

Exploring the Mechanism of Sempervirine Inhibiting Glioblastoma Invasion Based on Network Pharmacology and Bioinformatics.

Bingqiang Zhang, Wenyi Wang, Yu Song +7 more · 2024 · Pharmaceuticals (Basel, Switzerland) · MDPI · added 2026-04-24
📄 PDF DOI: 10.3390/ph17101318
DUSP6

TRIM11 expression levels was downregulated and prevents ferroptosis of cardiomyocyte by Dusp6 in acute myocardial infarction.

Xiaofu Wu, Wenyuan Zhang · 2024 · Anti-cancer drugs · added 2026-04-24
Acute myocardial infarction (AMI) is the high incidence rate and mortality of common cardiovascular disease. Herein, we explored the critical role of TRIM11 in AMI and its underlying mechanism. Serum Show more
Acute myocardial infarction (AMI) is the high incidence rate and mortality of common cardiovascular disease. Herein, we explored the critical role of TRIM11 in AMI and its underlying mechanism. Serum from patients with AMI were collected from our hospital. Mice of model group received angiotensin II. Mice of model + TRIM11 group received with Ang II and TRIM11 vectors. Mice of sham group received normal saline. H9c2 cells were performed transfections using Lipofectamine 2000 (Thermo Fisher Scientific Inc, Shanghai, China), and treated with Ang II. TRIM11 mRNA expression was reduced, was negative correlation with collagen I/III mRNA expression, systolic blood pressure, diastolic blood pressure, left anteroposterior atrial diameter, right atrial diameter, or left ventricular ejection fraction in patient with AMI. TRIM11 mRNA and protein expression were also suppressed. METTL3 regulates TRIM11 methylation to reduce TRIM11 gene stability in model of AMI. TRIM11 gene ameliorated AMI in mice model. TRIM11 gene reduced reactive oxygen species production level of cardiomyocyte in-vitro model. TRIM11 gene reduced ferroptosis of cardiomyocyte in-vitro model. TRIM11 gene reduced ferroptosis by the inhibition of mitochondrial damage of cardiomyocyte in model of AMI. TRIM11 induced Dusp6 protein expression. Bioluminescence imaging showed that TRIM11 virus increased Dusp6 expression in heart tissue of mice model. The inhibition of Dusp6 reduced the effects of TRIM11 on ferroptosis of cardiomyocyte in model of AMI. In conclusion, this study demonstrates that TRIM11 improves AMI by regulating Dusp6 to inhibit ferroptosis of cardiomyocyte, and suggest a novel target for AMI. Show less
no PDF DOI: 10.1097/CAD.0000000000001614
DUSP6

Combination of an Autoantibody Panel and Alpha-Fetoprotein for Early Detection of Hepatitis B Virus-Associated Hepatocellular Carcinoma.

Yajing Shen, Jiajun Chen, Jinyu Wu +6 more · 2024 · Cancer prevention research (Philadelphia, Pa.) · added 2026-04-24
The purpose of this study was to identify biomarkers associated with hepatitis B virus-associated hepatocellular carcinoma (HBV-HCC) and to develop a new combination with good diagnostic performance. Show more
The purpose of this study was to identify biomarkers associated with hepatitis B virus-associated hepatocellular carcinoma (HBV-HCC) and to develop a new combination with good diagnostic performance. This study was divided into four phases: discovery, verification, validation, and modeling. A total of four candidate tumor-associated autoantibodies (TAAb; anti-ZIC2, anti-PCNA, anti-CDC37L1, and anti-DUSP6) were identified by human proteome microarray (52 samples) and bioinformatics analysis. Subsequently, these candidate TAAbs were further confirmed by indirect ELISA with two testing cohorts (120 samples for verification and 663 samples for validation). The AUC for these four TAAbs to identify patients with HBV-HCC from chronic hepatitis B (CHB) patients ranged from 0.693 to 0.739. Finally, a diagnostic panel with three TAAbs (anti-ZIC2, anti-CDC37L1, and anti-DUSP6) was developed. This panel showed superior diagnostic efficiency in identifying early HBV-HCC compared with alpha-fetoprotein (AFP), with an AUC of 0.834 [95% confidence interval (CI), 0.772-0.897] for this panel and 0.727 (95% CI, 0.642-0.812) for AFP (P = 0.0359). In addition, the AUC for this panel to identify AFP-negative patients with HBV-HCC was 0.796 (95% CI, 0.734-0.858), with a sensitivity of 52.4% and a specificity of 89.0%. Importantly, the panel in combination with AFP significantly increased the positive rate for early HBV-HCC to 84.1% (P = 0.005) and for late HBV-HCC to 96.3% (P < 0.001). Our findings suggest that AFP and the autoantibody panel may be independent but complementary serologic biomarkers for HBV-HCC detection. We developed a robust diagnostic panel for identifying patients with HBV-HCC from patients with CHB. This autoantibody panel provided superior diagnostic performance for HBV-HCC at an early stage and/or with negative AFP results. Our findings suggest that AFP and the autoantibody panel may be independent but complementary biomarkers for HBV-HCC detection. Show less
no PDF DOI: 10.1158/1940-6207.CAPR-23-0311
DUSP6

Critical Role of miR-130b-5p in Cardiomyocyte Proliferation and Cardiac Repair in Mice After Myocardial Infarction.

Ke Feng, Yukang Wu, Jianguo Li +5 more · 2024 · Stem cells (Dayton, Ohio) · Oxford University Press · added 2026-04-24
Poor proliferative capacity of adult cardiomyocytes is the primary cause of heart failure after myocardial infarction (MI), thus exploring the molecules and mechanisms that promote the proliferation o Show more
Poor proliferative capacity of adult cardiomyocytes is the primary cause of heart failure after myocardial infarction (MI), thus exploring the molecules and mechanisms that promote the proliferation of adult cardiomyocytes is crucially useful for cardiac repair after MI. Here, we found that miR-130b-5p was highly expressed in mouse embryonic and neonatal hearts and able to promote cardiomyocyte proliferation both in vitro and in vivo. Mechanistic studies revealed that miR-130b-5p mainly promoted the cardiomyocyte proliferation through the MAPK-ERK signaling pathway, and the dual-specific phosphatase 6 (Dusp6), a negative regulator of the MAPK-ERK signaling, was the direct target of miR-130b-5p. Moreover, we found that overexpression of miR-130b-5p could promote the proliferation of cardiomyocytes and improve cardiac function in mice after MI. These studies thus revealed the critical role of miR-130b-5p and its targeted MAPK-ERK signaling in the cardiomyocyte proliferation of adult hearts and proved that miR-130b-5p could be a potential target for cardiac repair after MI. Show less
no PDF DOI: 10.1093/stmcls/sxad080
DUSP6

Hsa_Circ₀₀₀₈₀₃₅ drives immune evasion of gastric cancer via promoting EXT1-mediated nuclear translocation of PKM2.

Rongqi Jiang, Ping Li, Enqing Meng +3 more · 2024 · Translational oncology · Elsevier · added 2026-04-24
Circular RNAs (circRNAs) have been reported to be associated with the malignant phenotypes of cancer. However, the role and underlying mechanism of hsa_Circ₀₀₀₈₀₃₅ in colorectal cancer (CRC) remains Show more
Circular RNAs (circRNAs) have been reported to be associated with the malignant phenotypes of cancer. However, the role and underlying mechanism of hsa_Circ₀₀₀₈₀₃₅ in colorectal cancer (CRC) remains unclear. In this study, we elucidated the pivotal role of hsa_circ₀₀₀₈₀₃₅ in gastric cancer progression and immune evasion. Elevated hsa_circ₀₀₀₈₀₃₅ levels in gastric cancer patient serum correlated positively with disease advancement, including tumor stages and lymph node metastasis. Functional analyses revealed a negative association between hsa_circ₀₀₀₈₀₃₅ and CD8+ T cell number and function. Mechanistically, hsa_circ₀₀₀₈₀₃₅ encoded the novel protein EXT1-219aa, suppressing EXT1 phosphorylation and expression. Additionally, hsa_circ₀₀₀₈₀₃₅ regulated pyruvate metabolism by influencing the nucleus localization of PKM2. The identified EXT1/PKM2 axis further underscored the intricate regulatory mechanisms orchestrated by hsa_circ₀₀₀₈₀₃₅ in gastric cancer, offering potential diagnostic and therapeutic implications in the ongoing pursuit of targeted therapies for gastric cancer patients. Show less
📄 PDF DOI: 10.1016/j.tranon.2024.102004
EXT1

Temporal Transcriptome Dynamics of

Yuan Liu, Xianfeng Wu, Qian Xu +2 more · 2024 · Animals : an open access journal from MDPI · MDPI · added 2026-04-24
In this study, we measured the growth performance and intramuscular fat (IMF) content of the
📄 PDF DOI: 10.3390/ani14121770
FADS1

The potential molecular mechanism underlying gypenoside amelioration of atherosclerosis in ApoE

Xing Ju, Yufeng Liu, Ying Wang +9 more · 2024 · Heliyon · Elsevier · added 2026-04-24
Gypenosides (Gyp) are bioactive components of
📄 PDF DOI: 10.1016/j.heliyon.2024.e29164
FADS1

Brain tissue- and cell type-specific eQTL Mendelian randomization reveals efficacy of FADS1 and FADS2 on cognitive function.

Xueyan Wu, Lei Jiang, Hongyan Qi +16 more · 2024 · Translational psychiatry · Nature · added 2026-04-24
Epidemiological studies suggested an association between omega-3 fatty acids and cognitive function. However, the causal role of the fatty acid desaturase (FADS) gene, which play a key role in regulat Show more
Epidemiological studies suggested an association between omega-3 fatty acids and cognitive function. However, the causal role of the fatty acid desaturase (FADS) gene, which play a key role in regulating omega-3 fatty acids biosynthesis, on cognitive function is unclear. Hence, we used two-sample Mendelian randomization (MR) to estimate the gene-specific causal effect of omega-3 fatty acids (N = 114,999) on cognitive function (N = 300,486). Tissue- and cell type-specific effects of FADS1/FADS2 expression on cognitive function were estimated using brain tissue cis-expression quantitative trait loci (cis-eQTL) datasets (GTEx, N ≤ 209; MetaBrain, N ≤ 8,613) and single cell cis-eQTL data (N = 373), respectively. These causal effects were further evaluated in whole blood cis-eQTL data (N ≤ 31,684). A series of sensitivity analyses were conducted to validate MR assumptions. Leave-one-out MR showed a FADS gene-specific effect of omega-3 fatty acids on cognitive function [β = -1.3 × 10 Show less
📄 PDF DOI: 10.1038/s41398-024-02784-4
FADS1

Low-energy extracorporeal shockwave therapy improves locomotor functions, tissue regeneration, and modulating the inflammation induced FGF1 and FGF2 signaling to protect damaged tissue in spinal cord injury of rat model: an experimental animal study.

Chieh-Cheng Hsu, Kay L H Wu, Jei-Ming Peng +4 more · 2024 · International journal of surgery (London, England) · added 2026-04-24
Spinal cord injury (SCI) is a debilitating condition that results in severe motor function impairments. Current therapeutic options remain limited, underscoring the need for novel treatments. Extracor Show more
Spinal cord injury (SCI) is a debilitating condition that results in severe motor function impairments. Current therapeutic options remain limited, underscoring the need for novel treatments. Extracorporeal shockwave therapy (ESWT) has emerged as a promising noninvasive approach for treating musculoskeletal disorders and nerve regeneration. This study explored the effects of low-energy ESWT on locomotor function, tissue regeneration, inflammation, and mitochondrial function in a rat SCI model. Experiments were performed using locomotor function assays, CatWalk gait analysis, histopathological examination, immunohistochemical, and immunofluorescence staining. The findings demonstrated that low-energy ESWT had a dose-dependent effect, with three treatment sessions (ESWT3) showing superior outcomes compared to a single session. ESWT3 significantly improved motor functions [run patterns, run average speed, and maximum variation, as well as the Basso, Beattie, and Bresnahan score] and promoted tissue regeneration while reducing inflammation. ESWT3 significantly decreased levels of IL-1β, IL6, and macrophages (CD68) while increasing leukocyte (CD45) infiltration. Additionally, ESWT3 upregulated NueN and mitofusin 2 (MFN2), suggesting enhanced neuronal health and mitochondrial function. Moreover, ESWT3 modulated the expression of fibroblast growth factor 1 (FGF1), FGF2, their receptor FGFR1 and phosphorylation of ERK, aiding tissue repair, and regeneration in SCI. This study highlights the potential of low-energy ESWT as an effective noninvasive treatment for SCI, demonstrating significant improvements in motor recovery, tissue regeneration, anti-inflammatory effects, and mitochondrial protection. These findings provide valuable insights into the mechanisms of ESWT and its therapeutic application for SCI recovery. Show less
📄 PDF DOI: 10.1097/JS9.0000000000002128
FGFR1

FGFR1-mediated enhancement of foot-and-mouth disease virus entry.

Xuefei Wang, Ying Liao, Sahibzada Waheed Abdullah +7 more · 2024 · Veterinary microbiology · Elsevier · added 2026-04-24
Foot-and-mouth disease virus (FMDV), a member of picornavirus, can enter into host cell via macropinocytosis. Although it is known that receptor tyrosine kinases (RTKs) play a crucial role in FMDV mac Show more
Foot-and-mouth disease virus (FMDV), a member of picornavirus, can enter into host cell via macropinocytosis. Although it is known that receptor tyrosine kinases (RTKs) play a crucial role in FMDV macropinocytic entry, the specific RTK responsible for regulating this process and the intricacies of RTK-mediated downstream signaling remain to be elucidated. Here, we conducted a screening of RTK inhibitors to assess their efficacy against FMDV. Our findings revealed that two compounds specifically targeting fibroblast growth factor receptor 1 (FGFR1) and FMS-like tyrosine kinase 3 (FLT3) significantly disrupted FMDV entry. Furthermore, additional evaluation through gene knockdown and overexpression confirmed the promotion effect of FGFR1 and FLT3 on FMDV entry. Interestingly, we discovered that the increasement of FMDV entry facilitated by FGFR1 and FLT3 can be ascribed to increased macropinocytic uptake. Additionally, in-depth mechanistic study demonstrated that FGFR1 interacts with FMDV VP3 and undergoes phosphorylation during FMDV entry. Furthermore, the FGFR1 inhibitor inhibited FMDV-induced activation of p21-activated kinase 1 (PAK1) on Thr212 and Thr423 sites. Consistent with these findings, the ectopic expression of FGFR1 resulted in a concomitant increase in phosphorylation level of PAK1 on Thr212 and Thr423 sites. Taken together, our findings represent the initial exploration of FGFR1's involvement in FMDV macropinocytic entry, providing novel insights with potential implications for the development of antiviral strategies. Show less
no PDF DOI: 10.1016/j.vetmic.2024.110237
FGFR1

Dissecting the Distinct Tumor Microenvironments of HRD and HRP Ovarian Cancer: Implications for Targeted Therapies to Overcome PARPi Resistance in HRD Tumors and Refractoriness in HRP Tumors.

Junjun Qiu, Tingting Ren, Qinqin Liu +7 more · 2024 · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · Wiley · added 2026-04-24
High-grade serous tubo-ovarian cancer (HGSTOC) is an aggressive gynecological malignancy including homologous recombination deficient (HRD) and homologous recombination proficient (HRP) groups. Despit Show more
High-grade serous tubo-ovarian cancer (HGSTOC) is an aggressive gynecological malignancy including homologous recombination deficient (HRD) and homologous recombination proficient (HRP) groups. Despite the therapeutic potential of poly (ADP-ribose) polymerase inhibitors (PARPis) and anti-PDCD1 antibodies, acquired resistance in HRD and suboptimal response in HRP patients necessitate more precise treatment. Herein, single-cell RNA and single-cell T-cell receptor sequencing on 5 HRD and 3 HRP tumors are performed to decipher the heterogeneous tumor immune microenvironment (TIME), along with multiplex immunohistochemistry staining and animal experiments for validation. HRD tumors are enriched with immunogenic epithelial cells, FGFR1+PDGFRβ+ myCAFs, M1 macrophages, tumor reactive CD8+/CD4+ Tregs, whereas HRP tumors are enriched with HDAC1-expressing epithelial cells, indolent CAFs, M2 macrophages, and bystander CD4+/CD8+ T cells. Significantly, customized therapies are proposed. For HRD patients, targeting FGFR1+PDGFRβ+ myCAFs via tyrosine kinase inhibitors, targeting Tregs via anti-CCR8 antibodies/TNFRSF4 stimulation, and targeting CXCL13+ exhausted T cells by blocking PDCD1/CTLA-4/LAG-3/TIGIT are proposed. For HRP patients, targeting indolent CAFs, targeting M2 macrophages via CSF-1/CSF-1R inhibitors, targeting bystander T cells via tumor vaccines, and targeting epithelial cells via HDAC inhibitors. The study provides comprehensive insights into HRD and HRP TIME and tailored therapeutic approaches, addressing the challenges of PARPi-resistant HRD and refractory HRP tumors. Show less
📄 PDF DOI: 10.1002/advs.202309755
FGFR1

Fgf9 regulates bone marrow mesenchymal stem cell fate and bone-fat balance in osteoporosis by PI3K/AKT/Hippo and MEK/ERK signaling.

Mingmei Chen, Hui Liang, Min Wu +8 more · 2024 · International journal of biological sciences · added 2026-04-24
Bone-fat balance is crucial to maintain bone homeostasis. As common progenitor cells of osteoblasts and adipocytes, bone marrow mesenchymal stem cells (BMSCs) are delicately balanced for their differe Show more
Bone-fat balance is crucial to maintain bone homeostasis. As common progenitor cells of osteoblasts and adipocytes, bone marrow mesenchymal stem cells (BMSCs) are delicately balanced for their differentiation commitment. However, the exact mechanisms governing BMSC cell fate are unclear. In this study, we discovered that fibroblast growth factor 9 ( Show less
📄 PDF DOI: 10.7150/ijbs.94863
FGFR1

PKM2/Hif-1α signal suppression involved in therapeutics of pulmonary fibrosis with microcystin-RR but not with pirfenidone.

Yan Ren, Jie Wang, Wen-Wen Guo +4 more · 2024 · Toxicon : official journal of the International Society on Toxinology · Elsevier · added 2026-04-24
To date there are only pirfenidone (PFD) and nintedanib to be given conditional recommendation in idiopathic pulmonary fibrosis (IPF) therapies with slowing disease progression, but neither has prospe Show more
To date there are only pirfenidone (PFD) and nintedanib to be given conditional recommendation in idiopathic pulmonary fibrosis (IPF) therapies with slowing disease progression, but neither has prospectively shown a reduced mortality. It is one of the urgent topics to find effective drugs for pulmonary fibrosis in medicine. Previous studies have demonstrated that microcystin-RR (MC-RR) effectively alleviates bleomycin-induced pulmonary fibrosis, but the mechanism has not been fully elucidated yet. We further conducted a comparison of therapeutic effect on the model animals of pulmonary fibrosis between MC-RR and PFD with histopathology and the expression of the molecular markers involved in differentiation, proliferation and metabolism of myofibroblasts, a major effector cell of tissue fibrosis. The levels of the enzyme molecules for maintaining the stability of interstitial structure were also evaluated. Our results showed that MC-RR and PFD effectively alleviated pulmonary fibrosis in model mice with a decreased signaling and marker molecules associated with myofibroblast differentiation and lung fibrotic lesion. In the meantime, both MC-RR and PFD treatment are beneficial to restore molecular dynamics of interstitial tissue and maintain the stability of interstitial architecture. Unexpectedly, MC-RR, rather than PFD, showed a significant effect on inhibiting PKM2-HIF-1α signaling and reducing the level of p-STAT3. Additionally, MC-RR showed a better inhibition effect on FGFR1 expression. Given that PKM2-HIF-1α and activated STAT3 molecular present a critical role in promoting the proliferation of myofibroblasts, MC-RR as a new strategy for IPF treatment has potential advantage over PFD. Show less
no PDF DOI: 10.1016/j.toxicon.2024.107822
FGFR1

Somatic

Zekui Fang, Xiping Wu, Li Xiao +8 more · 2024 · Journal of thoracic disease · added 2026-04-24
The significant progress has been made in targeted therapy for lung adenocarcinoma (LUAD) in the past decade. Only few targeted therapeutics have yet been approved for the treatment of lung squamous c Show more
The significant progress has been made in targeted therapy for lung adenocarcinoma (LUAD) in the past decade. Only few targeted therapeutics have yet been approved for the treatment of lung squamous cell carcinoma (LUSC). Several higher frequency of gene alterations are identified as potentially actionable in LUSC. Our work aimed to explore the complex interplay of multiple genetic alterations and pathways contributing to the pathogenesis of LUSC, with a very low frequency of a single driver molecular alterations to develop more effective therapeutic strategies in the future. We retrospectively analyzed the targeted next-generation sequencing (NGS) data (approximately 600 genes) of 335 patients initially diagnosed with non-small cell lung cancer (NSCLC) at our institution between January 2019 and March 2023 and explored the somatic genome alteration difference between LUSC and LUAD. We analyzed that the presence of loss-of-function (LoF) mutations (nonsense, frameshift, and splice-site variants) in histone-lysine N-methyltransferase 2D ( Our results prompted that somatic LoF mutations of Show less
📄 PDF DOI: 10.21037/jtd-24-134
FGFR1

Synthesis and Anti-gastric Cancer Activity by Targeting FGFR1 Pathway of Novel Asymmetric Bis-chalcone Compounds.

Chunhui Nian, Xin Gan, Qunpeng Liu +10 more · 2024 · Current medicinal chemistry · Bentham Science · added 2026-04-24
Bis-chalcone compounds with symmetrical structures, either isolated from natural products or chemically synthesized, have multiple pharmacological activities. Asymmetric Bis-chalcone compounds have no Show more
Bis-chalcone compounds with symmetrical structures, either isolated from natural products or chemically synthesized, have multiple pharmacological activities. Asymmetric Bis-chalcone compounds have not been reported before, which might be attributed to the synthetic challenges involved, and it remains unknown whether these compounds possess any potential pharmacological activities. The aim of this study is to investigate the synthesis route of asymmetric bis-chalcone compounds and identify potential candidates with efficient anti-tumor activity. The two-step structural optimization of the bis-chalcone compounds was carried out sequentially, guided by the screening of the compounds for their growth inhibitory activity against gastric cancer cells by MTT assay. The QSAR model of compounds was established through random forest (RF) algorithm. The activities of the optimal compound J3 on growth inhibition, apoptosis, and apoptosis-inducing protein expression in gastric cancer cells were investigated sequentially by colony formation assay, flow cytometry, and western blotting. Further, the inhibitory effects of J3 on the FGFR1 signaling pathway were explored by Western Blotting, shRNA, and MTT assays. Finally, the 27 asymmetric bis-chalcone compounds, including two types (N and J) were sequentially designed and synthesized. Some N-class compounds have good inhibitory activity on the growth of gastric cancer cells. The vast majority of J-class compounds optimized on the basis of N3 exhibit excellent inhibitory activity on gastric cancer cell growth. We established a QSAR model (R In summary, this study outlines a viable method for the synthesis of novel asymmetric bischalcone compounds. Furthermore, the compound J3 demonstrates substantial promise as a potential candidate for an anti-tumor drug. Show less
no PDF DOI: 10.2174/0109298673298420240530093525
FGFR1

Macrophage-derived FGFR1 drives atherosclerosis through PLCγ-mediated activation of NF-κB inflammatory signalling pathway.

Lintao Wang, Wu Luo, Suya Zhang +11 more · 2024 · Cardiovascular research · Oxford University Press · added 2026-04-24
Atherosclerosis (AS) is a leading cause of cardiovascular morbidity and mortality. Atherosclerotic lesions show increased levels of proteins associated with the fibroblast growth factor receptor (FGFR Show more
Atherosclerosis (AS) is a leading cause of cardiovascular morbidity and mortality. Atherosclerotic lesions show increased levels of proteins associated with the fibroblast growth factor receptor (FGFR) pathway. However, the functional significance and mechanisms governed by FGFR signalling in AS are not known. In the present study, we investigated fibroblast growth factor receptor 1 (FGFR1) signalling in AS development and progression. Examination of human atherosclerotic lesions and aortas of Apoe-/- mice fed a high-fat diet (HFD) showed increased levels of FGFR1 in macrophages. We deleted myeloid-expressed Fgfr1 in Apoe-/- mice and showed that Fgfr1 deficiency reduces atherosclerotic lesions and lipid accumulations in both male and female mice upon HFD feeding. These protective effects of myeloid Fgfr1 deficiency were also observed when mice with intact FGFR1 were treated with FGFR inhibitor AZD4547. To understand the mechanistic basis of this protection, we harvested macrophages from mice and show that FGFR1 is required for macrophage inflammatory responses and uptake of oxidized LDL. RNA sequencing showed that FGFR1 activity is mediated through phospholipase-C-gamma (PLCγ) and the activation of nuclear factor-κB (NF-κB) but is independent of FGFR substrate 2. Our study provides evidence of a new FGFR1-PLCγ-NF-κB axis in macrophages in inflammatory AS, supporting FGFR1 as a potentially therapeutic target for AS-related diseases. Show less
no PDF DOI: 10.1093/cvr/cvae131
FGFR1

Evaluation of molecular residual disease in operable non-small cell lung cancer with gene fusions, MET exon skipping or de novo MET amplification.

Rui Fu, Yuanyuan Xiong, Miao Cai +4 more · 2024 · Frontiers of medicine · Springer · added 2026-04-24
Gene fusions and MET alterations are rare and difficult to detect in plasma samples. The clinical detection efficacy of molecular residual disease (MRD) based on circulating tumor DNA (ctDNA) in patie Show more
Gene fusions and MET alterations are rare and difficult to detect in plasma samples. The clinical detection efficacy of molecular residual disease (MRD) based on circulating tumor DNA (ctDNA) in patients with non-small cell lung cancer (NSCLC) with these mutations remains unknown. This prospective, non-intervention study recruited 49 patients with operable NSCLC with actionable gene fusions (ALK, ROS1, RET, and FGFR1), MET exon 14 skipping or de novo MET amplification. We analyzed 43 tumor tissues and 111 serial perioperative plasma samples using 1021- and 338-gene panels, respectively. Detectable MRD correlated with a significantly higher recurrence rate (P < 0.001), yielding positive predictive values of 100% and 90.9%, and negative predictive values of 82.4% and 86.4% at landmark and longitudinal time points, respectively. Patients with detectable MRD showed reduced disease-free survival (DFS) compared to those with undetectable MRD (P < 0.001). Patients who harbored tissue-derived fusion/MET alterations in their MRD had reduced DFS compared to those who did not (P = 0.05). To our knowledge, this is the first comprehensive study on ctDNA-MRD clinical detection efficacy in operable NSCLC patients with gene fusions and MET alterations. Patients with detectable tissue-derived fusion/MET alterations in postoperative MRD had worse clinical outcomes. Show less
📄 PDF DOI: 10.1007/s11684-024-1060-z
FGFR1

Discovery of LHQ490 as a highly selective fibroblast growth factor receptor 2 (FGFR2) inhibitor.

Huiqiong Li, Ran Ke, Yang Zhou +8 more · 2024 · European journal of medicinal chemistry · Elsevier · added 2026-04-24
Fibroblast growth factor receptor 2 (FGFR2) represents an appealing therapeutic target for multiple cancers, yet no selective FGFR2 inhibitors have been approved for clinical use to date. Here, we rep Show more
Fibroblast growth factor receptor 2 (FGFR2) represents an appealing therapeutic target for multiple cancers, yet no selective FGFR2 inhibitors have been approved for clinical use to date. Here, we report the discovery of a series of new selective, irreversible FGFR2 inhibitors. The representative compound LHQ490 potently inhibited FGFR2 kinase activity with an IC Show less
no PDF DOI: 10.1016/j.ejmech.2024.116473
FGFR1

Glucosamine Enhancement of Learning and Memory Functions by Promoting Fibroblast Growth Factor 21 Production.

Yu-Ming Chao, Hon-Yen Wu, Sin-Huei Yeh +3 more · 2024 · International journal of molecular sciences · MDPI · added 2026-04-24
Fibroblast growth factor 21 (FGF21) plays a crucial role in metabolism and brain function. Glucosamine (GLN) has been recognized for its diverse beneficial effects. This study aimed to elucidate the m Show more
Fibroblast growth factor 21 (FGF21) plays a crucial role in metabolism and brain function. Glucosamine (GLN) has been recognized for its diverse beneficial effects. This study aimed to elucidate the modulation of FGF21 production by GLN and its impact on learning and memory functions. Using both in vivo and in vitro models, we investigated the effects of GLN on mice fed with a normal diet or high-fat diet and on mouse HT22 hippocampal cells, STHdh Show less
📄 PDF DOI: 10.3390/ijms25084211
FGFR1

Dapagliflozin promotes browning of white adipose tissue through the FGFR1-LKB1-AMPK signaling pathway.

Yue Lv, Chengrui Zhao, Qiuyan Jiang +7 more · 2024 · Molecular biology reports · Springer · added 2026-04-24
Obesity is associated with a wide variety of metabolic disorders that impose significant burdens on patients and society. The "browning" phenomenon in white adipose tissue (WAT) has emerged as a promi Show more
Obesity is associated with a wide variety of metabolic disorders that impose significant burdens on patients and society. The "browning" phenomenon in white adipose tissue (WAT) has emerged as a promising therapeutic strategy to combat metabolic disturbances. However, though the anti-diabetic drug dapagliflozin (DAPA) is thought to promote "browning," the specific mechanism of this was previously unclear. In this study, C57BL/6 J male mice were used to establish an obesity model by high-fat diet feeding, and 3T3-L1 cells were used to induce mature adipocytes and to explore the role and mechanism of DAPA in "browning" through a combination of in vitro and in vivo experiments. The results show that DAPA promotes WAT "browning" and improves metabolic disorders. Furthermore, we discovered that DAPA activated "browning" through the fibroblast growth factor receptors 1-liver kinase B1-adenosine monophosphate-activated protein kinase signaling pathway. These findings provide a rational basis for the use of DAPA in treating obesity by promoting the browning of white adipose tissue. Show less
📄 PDF DOI: 10.1007/s11033-024-09540-3
FGFR1

Hyperglycemia activates FGFR1

Xiong Chen, Jinfu Qian, Shiqi Liang +8 more · 2024 · Acta pharmaceutica Sinica. B · Elsevier · added 2026-04-24
Protein tyrosine kinases (RTKs) modulate a wide range of pathophysiological events in several non-malignant disorders, including diabetic complications. To find new targets driving the development of Show more
Protein tyrosine kinases (RTKs) modulate a wide range of pathophysiological events in several non-malignant disorders, including diabetic complications. To find new targets driving the development of diabetic cardiomyopathy (DCM), we profiled an RTKs phosphorylation array in diabetic mouse hearts and identified increased phosphorylated fibroblast growth factor receptor 1 (p-FGFR1) levels in cardiomyocytes, indicating that FGFR1 may contribute to the pathogenesis of DCM. Using primary cardiomyocytes and H9C2 cell lines, we discovered that high-concentration glucose (HG) transactivates FGFR1 kinase domain through toll-like receptor 4 (TLR4) and c-Src, independent of FGF ligands. Knocking down the levels of either TLR4 or c-Src prevents HG-activated FGFR1 in cardiomyocytes. RNA-sequencing analysis indicates that the elevated FGFR1 activity induces pro-inflammatory responses Show less
📄 PDF DOI: 10.1016/j.apsb.2024.01.013
FGFR1

Circular RNA circTATDN3 promotes the Warburg effect and proliferation in colorectal cancer.

Jiatong Lin, Wenhui Zhong, Zejian Lyu +10 more · 2024 · Cancer letters · Elsevier · added 2026-04-24
As one of the key metabolic enzymes in the glycolytic pathway, lactate dehydrogenase A (LDHA) might be linked to tumor proliferation by driving the Warburg effect. Circular RNAs (circRNAs) are widely Show more
As one of the key metabolic enzymes in the glycolytic pathway, lactate dehydrogenase A (LDHA) might be linked to tumor proliferation by driving the Warburg effect. Circular RNAs (circRNAs) are widely implicated in tumor progression. Here, we report that circTATDN3, a circular RNA that interacts with LDHA, plays a critical role in proliferation and energy metabolism in CRC. We found that circTATDN3 expression was increased in CRC cells and tumor tissues and that high circTATDN3 expression was positively associated with poor postoperative prognosis in CRC patients. Additionally, circTATDN3 promoted the proliferation of CRC cells in vivo and vitro. Mechanistically, circTATDN3 was shown to function as an adaptor molecule that enhances the binding of LDHA to FGFR1, leading to increased LDHA phosphorylation and consequently promoting the Warburg effect. Moreover, circTATDN3 increased the expression of LDHA by sponging miR-511-5p, which synergistically promoted CRC progression and the Warburg effect. In conclusion, circTATDN3 may be a target for the treatment of CRC. Show less
no PDF DOI: 10.1016/j.canlet.2024.216825
FGFR1

The occurrence and development of abdominal aortic aneurysm may be related to the energy metabolism disorder and local inflammation.

Jun Li, Yang Liu, Zhitao Wei +2 more · 2024 · Heliyon · Elsevier · added 2026-04-24
The cellular mechanism of the formation of abdominal aortic aneurysm (AAA) is very complicated. A series of sophisticated events eventually led to significant pathological changes in the anatomical st Show more
The cellular mechanism of the formation of abdominal aortic aneurysm (AAA) is very complicated. A series of sophisticated events eventually led to significant pathological changes in the anatomical structure and function of the arterial wall and they are still not clear nowadays. We pooled publicly available GEO datasets (GSE57691 and GSE47472) to get a comprehensive comparisons between normal tissues and AAA tissues to try to reveal molecular mechanism underlying the disease. Total 63 AAA samples and 18 normal tissue samples were compared and we fond that there were 784 significantly different gene (DEGs, threshold set as adjusted In the pathway enrichment, we found that FOXP3 related signaling pathways, inflammation-related cytokine signaling pathways, interleukin-8-CXCR1 related signaling pathways and VEGFA and FGFR1 related signal pathway were significantly enrichmented. In Weighted gene co-expression network analysis (WGCNA), we found that the key hub genes were significantly related to lipid catabolic metabolism, which further verified the possibility that AAA might relate to energy metabolism disorders. Based on the comprehensive analysis of previous high-throughput data and the validation of basic experiments, we found that the occurrence of AAA may be related to energy metabolism disorders and local inflammation. Show less
📄 PDF DOI: 10.1016/j.heliyon.2024.e27912
FGFR1