J
Jun Peng
Researcher at Central South University
Publications - 9
Citations - 206
Jun Peng is an academic researcher from Central South University. The author has contributed to research in topics: Reperfusion injury & Ischemia. The author has an hindex of 5, co-authored 9 publications receiving 73 citations.
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Journal ArticleDOI
Ferroptosis occurs in phase of reperfusion but not ischemia in rat heart following ischemia or ischemia/reperfusion
TL;DR: Intervention of ferroptosis exerts beneficial effects on reperfusion injury but not ischemic injury, laying a basis for precise therapy for patients with myocardial infarction.
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Targeting the pathways of regulated necrosis: a potential strategy for alleviation of cardio-cerebrovascular injury
TL;DR: Targeting the pathways of regulated necrosis pharmacologically or genetically could be an efficient strategy for reducing cardio-cerebrovascular injury.
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Inhibition of Phosphoglycerate Mutase 5 Reduces Necroptosis in Rat Hearts Following Ischemia/Reperfusion Through Suppression of Dynamin-Related Protein 1
Lang She,Hua Tu,Yin Zhuang Zhang,Li Jing Tang,Nian Sheng Li,Qi Lin Ma,Bin Liu,Qingjie Li,Xiu-Ju Luo,Jun Peng +9 more
TL;DR: Inhibition of PGAM5 can reduce necroptosis in I/R-treated rat hearts through suppression of Drp1; there is a positive feedback between RIPK1 and PG AM5, and PGAM 5 might serve as a novel therapeutic target for prevention of myocardial I/ R injury.
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Cell Death and Exosomes Regulation After Myocardial Infarction and Ischemia-Reperfusion.
TL;DR: In this article, the authors focused on introducing various cell-derived exosomes to reduce cell death after MI by regulating the cell death pathway to understand myocardial repair mechanisms better and provide a reference for clinical treatment.
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Suppression of NADPH oxidase attenuates hypoxia-induced dysfunctions of endothelial progenitor cells
TL;DR: It is concluded that NOX-derived ROS contributes to the dysfunctions of EPCs under hypoxic condition and suppression of NOX may provide a novel strategy to improve endothelial functions in hypoxia-relevant diseases.