The present review highlights the frequently underappreciated role of VSMCs in sepsis-induced vasodilation, and provides a comprehensive and systematic elucidation of the associated pathophysiological mechanisms.
First-pass extracted concept
vascular smooth muscle cell pathobiology in sepsis-induced vasoplegia
Candidate: concept label1 source documents7 linked claims
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In sepsis, pathogens can directly injure vascular smooth muscle cells.
Phenotypic switching of vascular smooth muscle cells in sepsis is associated with increased proliferative and migratory abilities.
Sepsis disrupts endothelial cell-vascular smooth muscle cell interactions and calcium homeostasis, contributing to reduced vascular reactivity and abnormal vascular remodeling.
The sepsis-associated cytokine storm can activate NF-κB and p38 MAPK signaling in vascular smooth muscle cells, promoting a shift from a contractile to a synthetic phenotype.
Combined vascular smooth muscle cell injury, inflammatory signaling, disrupted endothelial-vascular smooth muscle communication, and calcium dysregulation contribute to sepsis-related vascular dysfunction and multiorgan failure.
This review argues that vascular smooth muscle cells are an underappreciated contributor to sepsis-induced vasodilation and vasoplegia.
The review presents vascular smooth muscle cells as a theoretical target class for future clinical intervention strategies in sepsis.