Sepsis-Induced Endothelial Dysfunction: Permeability and Regulated Cell Death

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.