T
Tao Wen
Researcher at Capital Medical University
Publications - 51
Citations - 1497
Tao Wen is an academic researcher from Capital Medical University. The author has contributed to research in topics: Inflammation & Liver injury. The author has an hindex of 17, co-authored 48 publications receiving 844 citations. Previous affiliations of Tao Wen include Beijing Chao-Yang Hospital.
Papers
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Journal ArticleDOI
NRF2, a Transcription Factor for Stress Response and Beyond.
Feng He,Xiaoli Ru,Tao Wen +2 more
TL;DR: The complex regulatory network of NRF2 activity and its roles in metabolic reprogramming, unfolded protein response, proteostasis, autophagy, mitochondrial biogenesis, inflammation, and immunity are summarized.
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Peroxisome proliferator-activated receptor α activation attenuates the inflammatory response to protect the liver from acute failure by promoting the autophagy pathway
M Jiao,F Ren,Li Zhou,Xiangying Zhang,L Zhang,Tao Wen,Linlin Wei,Xia Wang,Honglin Shi,Lina Bai,Sujun Zheng,Jia Zhang,Yu Chen,Yuan-Ping Han,Caiyan Zhao,Zhongping Duan +15 more
TL;DR: It is demonstrated that PPARα-mediated induction of autophagy ameliorated liver injury in cases of ALF by attenuating inflammatory responses, indicating a potential therapeutic application for ALF treatment.
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Inhibition of glycogen synthase kinase 3β promotes autophagy to protect mice from acute liver failure mediated by peroxisome proliferator-activated receptor α.
F Ren,Linzhong Zhang,Linzhong Zhang,Xulong Zhang,Honglin Shi,Tao Wen,Lina Bai,Sujun Zheng,Yu Chen,De-Xi Chen,Liying Li,Zhongping Duan +11 more
TL;DR: The increased GSK3β activity suppresses autophagy to promote the occurrence and development of ALF by inhibiting PPARα pathway, which is a recently recognized rudimentary cellular response to inflammation and injury.
Journal ArticleDOI
DCLK1 is up-regulated and associated with metastasis and prognosis in colorectal cancer
TL;DR: DCLK1 up-regulation may play a contributory role in CRC metastasis and poor prognosis via activation of EMT and may serve as an independent predictor for CRC prognosis.
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Extracellular histones are clinically relevant mediators in the pathogenesis of acute respiratory distress syndrome.
TL;DR: Ex-vivo analysis showed that ARDS patient’s BALF remarkably induced epithelial and endothelial cell damage and stimulated cytokine production in the supernatant of U937 cells, suggesting that targeting extracellular histones may provide a promising approach for treating ARDS.