程序性细胞死亡
自噬
GPX4
脂质过氧化
细胞凋亡
再灌注损伤
发病机制
缺血
坏死
癌症研究
氧化应激
移植
细胞
生物
医学
细胞生物学
免疫学
内科学
病理
生物化学
超氧化物歧化酶
谷胱甘肽过氧化物酶
作者
Shanshan Guo,Zexin Li,Yi Liu,Ying Cheng,Degong Jia
标识
DOI:10.1080/10715762.2024.2386075
摘要
Ischemia-reperfusion injury (IRI) can seriously affect graft survival and prognosis and is an unavoidable event during liver transplantation. Ferroptosis is a novel iron-dependent form of cell death characterized by iron accumulation and overwhelming lipid peroxidation; it differs morphologically, genetically, and biochemically from other well-known cell death types (autophagy, necrosis, and apoptosis). Accumulating evidence has shown that ferroptosis is involved in the pathogenesis of hepatic IRI, and targeting ferroptosis may be a promising therapeutic approach. Here, we review the pathways and phenomena involved in ferroptosis, explore the associations and implications of ferroptosis and hepatic IRI, and discuss possible strategies for modulating ferroptosis to alleviate the hepatic IRI.
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