Molecular Mechanisms Governing Vascular Function in Heart Failure.

Authors

Valeria Garrido-Moreno, Anwarul Ferdous, Thomas G Gillette, Joseph A Hill

Published in

Arteriosclerosis, thrombosis, and vascular biology. Volume 46. Issue 10. Pages e323132. Epub Aug 20, 2026.

Abstract

Heart failure is a leading cause of morbidity and mortality worldwide. Emerging evidence points to vascular dysfunction as a major contributor to the development and progression of this grievous syndrome. Functional interplay between the myocardium and vasculature involves endothelial cells, vascular smooth muscle cells, and pericytes governing tissue perfusion, vascular tone, inflammation, and metabolism. Vascular cells play a central role in maintaining cardiovascular homeostasis by sensing hemodynamic and inflammatory stimuli and releasing vasoactive and paracrine factors. Dysregulation of endothelium-derived mediators such as NO, endothelin-1, and endothelium-derived hyperpolarizing factors, along with vascular oxidative stress, inflammation, and vascular remodeling (eg, disturbances in angiogenesis and microvascular rarefaction) impair myocardial perfusion and can accelerate heart failure progression. Here, we summarize key molecular mechanisms linking vascular dysfunction to heart failure, emphasizing endothelial signaling, oxidative stress, inflammation, and angiogenic remodeling.

PMID:
42619591
Bibliographic data and abstract were imported from PubMed on 15 Oct 2026.

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