Icariin inhibits hypoxia/reoxygenation‐induced ferroptosis of cardiomyocytes via regulation of the Nrf2/HO‐1 signaling pathway

• Published in: FEBS open bio Vol. 11; no. 11; pp. 2966 - 2976
• Main Authors: Liu, Xiu‐Juan, Lv, Yan‐Fei, Cui, Wen‐Zhu, Li, Yan, Liu, Yang, Xue, Yi‐Tao, Dong, Feng
• Format: Journal Article
• Language: English
• Published: England John Wiley & Sons, Inc 01.11.2021; John Wiley and Sons Inc; Wiley
• Subjects: Apoptosis; Apoptosis - drug effects; Bioengineering; Blood flow; Cardiomyocytes; Cell death; Cell Hypoxia - drug effects; Cell Hypoxia - physiology; Cell Line; Cell Survival - drug effects; Dehydrogenases; Endoplasmic reticulum; Ferroptosis; Flavonoids - metabolism; Flavonoids - pharmacology; Heart attacks; Hypoxia; Hypoxia - drug therapy; Hypoxia - metabolism; hypoxia/reoxygenation; icariin; Iron; Ischemia; L-Lactate dehydrogenase; lactate dehydrogenase; Lactic acid; Membranes; Myocardial infarction; Myocardial Reperfusion Injury - metabolism; Myocardium; Myocytes, Cardiac - drug effects; NF-E2-Related Factor 2 - drug effects; NF-E2-Related Factor 2 - metabolism; Nrf2/HO‐1 pathway; Oxidative stress; Oxidative Stress - drug effects; Plaques; protective effect; Proteins; Reactive oxygen species; Reactive Oxygen Species - metabolism; Signal transduction; Signal Transduction - drug effects; Software; viability; United States > US; China; Germany; cardiomyocytes; icariin; Nrf2/HO-1 pathway; ferroptosis; oxidative stress; hypoxia/reoxygenation

Myocardial infarction (MI) is caused by the formation of plaques in the arterial walls, leading to a decrease of blood flow to the heart and myocardium injury as a result of hypoxia. Ferroptosis is a crucial event in myocardial injury, and icariin (ICA) exerts protective effects against myocardial i...