The effects of sepsis on endothelium and clinical implications.

Abstract:

ABSTRACT:Sepsis accounts for nearly 700 000 deaths in Europe annually and is caused by an overwhelming host response to infection resulting in organ failure. The endothelium is an active contributor to sepsis and as such represents a major target for therapy. During sepsis, endothelial cells amplify the immune response and activate the coagulation system. They are both a target and source of inflammation and serve as a link between local and systemic immune responses. In response to cytokines produced by immune cells, the endothelium expresses adhesion molecules and produces vasoactive compounds, inflammatory cytokines, and chemoattractants, thus switching from an anticoagulant to procoagulant state. These responses contribute to local control of infection, but systemic activation can lead to microvascular thrombosis, capillary permeability, hypotension, tissue hypoxia, and ultimately tissue damage. This review focuses on the role of the endothelium in leucocyte adhesion and transmigration as well as production of reactive oxygen and nitrogen species, microRNAs and cytokines, formation of signalling microparticles, and disseminated intravascular coagulation. We also discuss alterations in endothelial permeability and apoptosis. Finally, we review the diagnostic potential of endothelial markers and endothelial pathways as therapeutic targets for this devastating disease.

journal_name

Cardiovasc Res

journal_title

Cardiovascular research

authors

Dolmatova EV,Wang K,Mandavilli R,Griendling KK

doi

10.1093/cvr/cvaa070

subject

Has Abstract

pub_date

2021-01-01 00:00:00

pages

60-73

issue

1

eissn

0008-6363

issn

1755-3245

pii

5811761

journal_volume

117

pub_type

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