自噬在对乙酰氨基酚诱导肝损伤中的作用
DOI: 10.12449/JCH250229
利益冲突声明:本文不存在任何利益冲突。
作者贡献声明:邢国静负责课题设计,撰写论文;王丽菲、罗龙龙负责归纳文献,分析资料;郑晓凤、高春、于晓辉参与修改论文;张久聪负责拟定写作思路,指导撰写文章并最后定稿。
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摘要: 对乙酰氨基酚(APAP)是临床上常用的解热镇痛药,过量服用则会造成严重肝损伤甚至死亡。近年来,APAP诱导的肝损伤(AILI)发生率呈上升趋势,已成为全球肝移植的第二大常见原因。自噬是一种高度保守的分解代谢过程,通过溶酶体降解去除不需要的胞质蛋白和细胞器,以实现细胞本身的代谢需要和细胞器的更新。大量研究表明,自噬在AILI的病理生理中起着关键作用,其机制涉及APAP蛋白加合物、氧化应激、JNK活化、线粒体功能障碍、炎症反应和细胞凋亡等。本文通过阐述自噬在AILI中的生物学机制,为AILI的治疗和自噬调节剂的开发提供理论依据。
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关键词:
- 自噬 /
- 醋氨酚 /
- 化学性与药物性肝损伤 /
- 病理过程
Abstract: N-acetyl-p-aminophenol (APAP) is an antipyretic analgesic commonly used in clinical practice, and APAP overdose can cause severe liver injury and even death. In recent years, the incidence rate of APAP-induced liver injury (AILI) tends to increase, and it has become the second most common cause of liver transplantation worldwide. Autophagy is a highly conserved catabolic process that removes unwanted cytosolic proteins and organelles through lysosomal degradation to achieve the metabolic needs of cells themselves and the renewal of organelles. A large number of studies have shown that autophagy plays a key role in the pathophysiology of AILI, involving the mechanisms such as APAP protein conjugates, oxidative stress, JNK activation, mitochondrial dysfunction, inflammatory response and apoptosis. This article elaborates on the biological mechanism of autophagy in AILI, in order to provide a theoretical basis for the treatment of AILI and the development of autophagy regulators.-
Key words:
- Autophagy /
- Acetaminophen /
- Chemical and Drug Indued Liver Injury /
- Pathologic Processes
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