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Xiao-Feng Zeng
Researcher at Wuhan University
Publications - 11
Citations - 292
Xiao-Feng Zeng is an academic researcher from Wuhan University. The author has contributed to research in topics: Inflammation & Cardiac fibrosis. The author has an hindex of 6, co-authored 8 publications receiving 164 citations.
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CTRP3 protected against doxorubicin-induced cardiac dysfunction, inflammation and cell death via activation of Sirt1.
TL;DR: Cardiac specific-overexpression of CTRP3 preserved heart dysfunction, and attenuated cardiac inflammation and cell loss induced by DOX in vivo and in vitro, showing therapeutic potential for the treatment of DOX cardiotoxicity.
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Andrographolide Protects Against Adverse Cardiac Remodeling After Myocardial Infarction through Enhancing Nrf2 Signaling Pathway.
Saiyang Xie,Wei Deng,Jiao-Jiao Chen,Qing-Qing Wu,Hongjian Li,Juan Wang,Li Wei,Chen Liu,Mingxia Duan,Zhulan Cai,Qingwen Xie,Tongtong Hu,Xiao-Feng Zeng,Qi-Zhu Tang +13 more
TL;DR: It is suggested that Andr alleviates adverse cardiac remodeling following myocardial infarction through enhancing Nrf2 signaling pathway.
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Mnk1 (Mitogen-Activated Protein Kinase-Interacting Kinase 1) Deficiency Aggravates Cardiac Remodeling in Mice
Yuan Yuan,Ling Yan,Qing-Qing Wu,Heng Zhou,Ya-Ge Jin,Zhou-Yan Bian,Wei Deng,Zheng Yang,Difei Shen,Xiao-Feng Zeng,Sha-Sha Wang,Hongliang Li,Qi-Zhu Tang +12 more
TL;DR: Mk1 likely carries out a suppressive function in cardiac hypertrophy via regulating the sprouty2/ERK1/2 pathway and exhibited signs of a blunted cardiac hypertrophic response.
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Overexpression of CTRP3 protects against sepsis-induced myocardial dysfunction in mice
TL;DR: Cardioprotective effects of CTRP3 might be mediated by activating AMPKα signaling pathway and blunting inflammatory response and apoptosis and could protect against sepsis-induced myocardial dysfunction in mice.
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Acacetin protects against cardiac remodeling after myocardial infarction by mediating MAPK and PI3K/Akt signal pathway.
TL;DR: Collectively, acacetin improves mouse left ventricular function and attenuates cardiac remodeling by inhibiting of the MAPK and PI3K/Akt signaling pathway.