Shared features of endothelial dysfunction between sepsis and its preceding risk factors (aging and chronic disease)

TL;DR

This review identifies shared features of endothelial dysfunction in sepsis, aging, and chronic diseases, highlighting common mechanisms like inflammation, glycocalyx degradation, and coagulation, which may influence sepsis development.

Contribution

The paper systematically reviews and compares endothelial dysfunction features across sepsis, aging, and chronic diseases, emphasizing their commonalities and potential impact on sepsis pathogenesis.

Findings

Shared features include increased oxidative stress and inflammation

Glycocalyx degradation and junction disassembly are common

Chronic diseases impair endothelial repair mechanisms

Abstract

Acute vascular endothelial dysfunction is a central event in the pathogenesis of sepsis,increasing vascular permeability, promoting activation of the coagulation cascade, tissue edema and compromising perfusion of vital organs. Aging and chronic diseases(hypertension,dyslipidaemia,diabetes mellitus,chronic kidney disease,cardiovascular disease,cerebrovascular disease, chronic pulmonary disease,liver disease or cancer)are recognized risk factors for sepsis. In this article we review the features of endothelial dysfunction shared by sepsis,aging and the chronic conditions preceding this disease. Clinical studies and review articles on endothelial dysfunction associated to sepsis,aging and chronic diseases published in PubMed were considered. The main features of endothelial dysfunction shared by sepsis,aging and chronic diseases were 1.increased oxidative stress and systemic inflammation, 2.glycocalyx degradation and shedding, 3.disassembly of intercellular junctions,endothelial cell death,blood tissue barrier disruption, 4.enhanced leukocyte adhesion and extravasation, 5.induction of a pro-coagulant and anti-fibrinolytic state. In addition,chronic diseases impair the mechanisms of endothelial reparation. In conclusion,sepsis,aging and chronic diseases induce similar features of endothelial dysfunction. The potential contribution of the pre-existent degree of endothelial dysfunction to sepsis pathogenesis deserves to be further investigated