BI1 alleviates cardiac microvascular ischemia‐reperfusion injury via modifying mitochondrial fission and inhibiting XO/ROS/F‐actin pathways

Pathogenesis of cardiac microvascular ischemia‐reperfusion (IR) injury is associated with excessive mitochondrial fission. However, the upstream mediator of mitochondrial fission remains obscure. Bax inhibitor 1 (BI1) is linked to multiple mitochondrial functions, and there have been no studies inve...

Ausführliche Beschreibung

Gespeichert in:

Bibliographische Detailangaben
Veröffentlicht in:	Journal of cellular physiology 2019-04, Vol.234 (4), p.5056-5069
Hauptverfasser:	Zhou, Hao, Wang, Jin, Hu, Shunying, Zhu, Hong, Toan, Sam, Ren, Jun
Format:	Artikel
Sprache:	eng
Schlagworte:	Actin Actins - metabolism Animals Apoptosis BI1 Cells, Cultured Depolymerization Deregulation Endothelial cells Fission F‐actin Heart Heart - physiopathology Homeostasis Injuries Ischemia Male Membrane Proteins - metabolism Mice Mice, Transgenic microvascular IR injury Microvasculature Mitochondria Mitochondria, Heart - metabolism Mitochondrial Dynamics - physiology mitochondrial fission Myocardial Ischemia - pathology Myocardial Reperfusion Injury - pathology Oxidative stress Oxidative Stress - physiology Pathogenesis Reactive oxygen species Reactive Oxygen Species - metabolism Reperfusion Viability Xanthine oxidase Xanthine Oxidase - metabolism
Online-Zugang:	Volltext
Tags:	Tag hinzufügen Keine Tags, Fügen Sie den ersten Tag hinzu!

Schreiben Sie den ersten Kommentar!