程序性细胞死亡
细胞凋亡
心力衰竭
GPX4
心肌梗塞
平衡
细胞
医学
氧化应激
细胞生物学
癌症研究
生物信息学
生物
内科学
生物化学
谷胱甘肽过氧化物酶
过氧化氢酶
作者
Xinquan Yang,Nicholas K. Kawasaki,Junxia Min,Takashi Matsui,Fudi Wang
标识
DOI:10.1016/j.yjmcc.2022.10.004
摘要
With its complicated pathobiology and pathophysiology, heart failure (HF) remains an increasingly prevalent epidemic that threatens global human health. Ferroptosis is a form of regulated cell death characterized by the iron-dependent lethal accumulation of lipid peroxides in the membrane system and is different from other types of cell death such as apoptosis and necrosis. Mounting evidence supports the claim that ferroptosis is mainly regulated by several biological pathways including iron handling, redox homeostasis, and lipid metabolism. Recently, ferroptosis has been identified to play an important role in HF induced by different stimuli such as myocardial infarction, myocardial ischemia reperfusion, chemotherapy, and others. Thus, it is of great significance to deeply explore the role of ferroptosis in HF, which might be a prerequisite to precise drug targets and novel therapeutic strategies based on ferroptosis-related medicine. Here, we review current knowledge on the link between ferroptosis and HF, followed by critical perspectives on the development and progression of ferroptotic signals and cardiac remodeling in HF.
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