👤 Changchen Wu

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