活性氧
自噬
脂质过氧化
GPX4
疾病
机制(生物学)
氧化应激
激活剂(遗传学)
程序性细胞死亡
细胞生物学
生物
细胞凋亡
癌症研究
医学
受体
生物化学
内科学
超氧化物歧化酶
哲学
谷胱甘肽过氧化物酶
认识论
作者
Yuhan Qin,Qiao Ye,Dong Wang,Chengchun Tang,Gaoliang Yan
标识
DOI:10.1016/j.biopha.2021.111872
摘要
Ferroptosis is a type of regulated cell death driven by iron dependent accumulation of cellular reactive oxygen species (ROS) when glutathione (GSH)-dependent lipid peroxidation repair systems are compromised. Nuclear receptor co-activator 4 (NCOA4)-mediated selective autophagy of ferritin, termed ferritinophagy, involves the regulation of ferroptosis. Emerging evidence has revealed that ferritinophagy and ferroptosis exert a significant role in the occurrence and development of cardiovascular disease. In the present review, we aimed to present a brief overview of ferritinophagy and ferroptosis focusing on the underlying mechanism and regulations involved. We summarize and discuss relevant research progress on the role of ferritinophagy and ferroptosis in cardiovascular diseases accompanied with potential applications of ferritinophagy and ferroptosis modulators in the treatment of ferroptosis-associated cardiovascular diseases.
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