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脓毒症诱导的内皮功能障碍:通透性与程序性细胞死亡

Sepsis-Induced Endothelial Dysfunction: Permeability and Regulated Cell Death.

作者信息

Zhang Wei, Jiang Luofeng, Tong Xirui, He Heng, Zheng Yongjun, Xia Zhaofan

机构信息

Department of Burn Surgery, the First Affiliated Hospital of Naval Medical University, Shanghai, 200433, People's Republic of China.

Research Unit of Key Techniques for Treatment of burns and Combined Burns and Trauma Injury, Chinese Academy of Medical Sciences, Shanghai, 200433, People's Republic of China.

出版信息

J Inflamm Res. 2024 Nov 28;17:9953-9973. doi: 10.2147/JIR.S479926. eCollection 2024.

Abstract

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Endothelial cells (ECs) are an important cell type typically affected in sepsis, resulting in compromised barrier function and various forms of regulated cell death (RCD). However, the precise mechanisms underlying sepsis-induced EC damage remain unclear. This review summarizes the recent research progress on factors and mechanisms that may affect the permeability and RCD of ECs under septic conditions, including glycocalyx, damage-associated molecular patterns, and various forms of RCD in ECs, such as apoptosis, pyroptosis, ferroptosis, and autophagy. This review offers important insights into the underlying mechanisms of endothelial dysfunction in sepsis, aiming to contribute to developing small-molecule targeted clinical therapies.

摘要

脓毒症是由宿主对感染的反应失调引起的危及生命的器官功能障碍。内皮细胞(ECs)是脓毒症中典型受影响的重要细胞类型,导致屏障功能受损和各种形式的程序性细胞死亡(RCD)。然而,脓毒症诱导的EC损伤的确切机制仍不清楚。本综述总结了脓毒症条件下可能影响ECs通透性和RCD的因素及机制的最新研究进展,包括糖萼、损伤相关分子模式以及ECs中的各种形式的RCD,如凋亡、焦亡、铁死亡和自噬。本综述为脓毒症内皮功能障碍的潜在机制提供了重要见解,旨在为开发小分子靶向临床治疗做出贡献。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af78/11612565/667bd909201c/JIR-17-9953-g0001.jpg

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