摘要
脓毒症是一类严重威胁全球人类健康的复杂疾病,以高发病率和高病死率为显著特征。在脓毒症继发的器官功能障碍中,心功能障碍是最常见的并发症之一,也是脓毒症患者死亡的主要原因。现有研究充分阐明细胞损伤、线粒体功能障碍和钙稳态在脓毒症心功能障碍中的关键作用。近年来,自噬作为维持细胞稳态的重要过程,在脓毒症心功能障碍中的作用引起了广泛关注。尽管部分研究提示自噬激活可能对脓毒症心功能障碍具有保护效应,但其是否可通过选择性降解上述病理机制中的信号分子,从而减缓心功能障碍进展,尚不明确。本文系统综述了自噬在脓毒症心功能障碍中的研究进展,梳理其主要信号通路及调控机制,旨在为揭示脓毒症心功能障碍的发病机制和探索潜在的治疗靶点提供理论支持。
Sepsis is a complex and life-threatening disorder characterized by high morbidity and case fatality rate,posing a significant global health challenge.Cardiac dysfunction represents one of the most prevalent complications in sepsis-induced multiorgan failure and serves as a leading cause of mortality in septic patients.Current studies have thoroughly elucidated the critical roles of cellular injury,mitochondrial dysfunction,and calcium homeostasis in sepsis-induced myocardial dysfunction(SIMD).In recent years,autophagy,as a critical process for maintaining cell homeostasis,has attracted increasing attention for its role in SIMD.Although emerging evidence suggests that autophagy activation may confer cardioprotective effects in SIMD,it remains unclear whether autophagy can selectively degrade signaling molecules involved in key pathological processes—such as cardiomyocyte injury,mitochondrial dysfunction,and calcium overload—to attenuate the progression of cardiac impairment.This article systematically reviews the research progress of autophagy in SIMD,sorts out its main signaling pathways and regulatory mechanisms,aiming to provide theoretical support for revealing the pathogenesis of SIMD and exploring potential therapeutic targets.
作者
毕成菲
李妍
胡韡
朱华栋
BI Chengfei;LI Yan;HU Wei;ZHU Huadong(Department of Emergency,the State Key Laboratory for Complex,Severe and Rare Diseases,Peking Union Medical College Hospital,Chinese Academy of Medical Science and Peking Union Medical College,Beijing,100730,China)
出处
《临床急诊杂志》
2026年第1期64-70,共7页
Journal of Clinical Emergency
基金
中央高水平医院临床科研项目(No:2022-PUMCH-B-109)。
关键词
脓毒症
心功能障碍
脓毒症心功能障碍
自噬
病理生理学机制
sepsis
myocardial dysfunction
sepsis-induced myocardial dysfunction
autophagy
pathophysiological mechanism
