摘要
自噬是真核细胞内广泛存在的一种依赖溶酶体对物质进行降解的过程，能维持细胞内稳态，对抗细胞损伤。自噬在急性肝衰竭发生发展中有重要保护作用，其机制涉及到肝组织氧化应激和内质网应激减轻、固有免疫炎性反应受抑和肝凋亡与肝再生平衡打破等。
Autophagy widely exists in eukaryotic cells. It is an intracellular catabolic process by which cytoplasmic material is delivered to lysosomes for degradation, which can help maintain cellular homeostasis and fight against cell damage. Recently, it has been found that autophagy plays important protective roles in acute liver failure, and the mechanisms are complicated. Understanding these protective effects and related molecular mechanisms are helpful to find new treatment strategies for acute liver failure. In this review, we summarize the protective effects and related molecular mechanisms of autophagy including oxidative stress reduction, innate immune inflammatory response inhibition, apoptosis inhibition and liver regeneration promotion.
作者
钟欢
何玉
谈志丽
刘亮明
ZHONG Huan;HE Yu;TAN Zhili;LIU Liangming(Department of Infectious Disease, Shanghai Songjiang Central Hospital Affiliated to Nanfing Medical University, Songjiang Branch of Shanghai First People＇ s Hospital Affiliated to Shanghai Jiaotong U- niversity, Shanghai, 201600, China)
出处
《医学分子生物学杂志》
CAS
2018年第2期110-113,124,共5页
Journal of Medical Molecular Biology
基金
国家自然科学基金（No.81770612,81070357,30660066）,上海市松江区科学技术攻关项目（No.16SJGG21）
关键词
急性肝衰竭
自噬
氧化应激
内质网应激
炎症
凋亡
肝再生
acute liver failure
autophagy
oxidative stress
endoplasmic reticulum stress
inflammation
apoptosis
liver regeneration
