c-FLIP通过FUNDC1介导的线粒体自噬调节保护脓毒症诱导的心肌功能障碍中的心脏微循环。
c-FLIP Protects Cardiac Microcirculation in Sepsis-Induced Myocardial Dysfunction Via FUNDC1-Mediated Regulation of Mitochondrial Autophagy.
作者信息
Gao Lan, Shi Qindong, Sun Bin, Zhang Xiaoyu, Zheng Peiying, Zhou Linjing, Tian Gang, Li Hao
机构信息
Department of Critical Care Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China; Shaanxi Provincial Key Laboratory of Sepsis in Critical Care Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Department of Critical Care Medicine, Qinghai Provincial People's Hospital, Xining, Qinghai, China.
出版信息
JACC Basic Transl Sci. 2025 Aug;10(8):101257. doi: 10.1016/j.jacbts.2025.02.016. Epub 2025 May 14.
This study investigates the role of c-FLIP in sepsis-induced myocardial dysfunction (SIMD), focusing on cardiac microcirculation and mitochondrial autophagy. Using SIMD rat and LPS-induced cardiac microvascular endothelial cell injury models, we found that c-FLIP deficiency disrupts mitochondrial homeostasis, exacerbating microcirculatory damage. c-FLIP differentially regulates mitochondrial autophagy via FUNDC1. Overexpression of c-FLIP balances autophagy, protects mitochondria, reduces inflammation, and ameliorates SIMD, highlighting its potential as a therapeutic target.
本研究调查了c-FLIP在脓毒症诱导的心肌功能障碍（SIMD）中的作用，重点关注心脏微循环和线粒体自噬。利用SIMD大鼠和脂多糖诱导的心脏微血管内皮细胞损伤模型，我们发现c-FLIP缺乏会破坏线粒体稳态，加剧微循环损伤。c-FLIP通过FUNDC1差异性地调节线粒体自噬。c-FLIP的过表达可平衡自噬、保护线粒体、减轻炎症并改善SIMD，突显了其作为治疗靶点的潜力。
Zotero 插件