Endothelial cell dysfunction in cardiac disease: driver or consequence?

Abstract

The vascular endothelium is a multifunctional cellular system which directly influences blood components and cells within the vessel wall in a given tissue. Importantly, this cellular interface undergoes critical phenotypic changes in response to various biochemical and hemodynamic stimuli, driving several developmental and pathophysiological processes. Multiple studies have indicated a central role of the endothelium in the initiation, progression, and clinical outcomes of cardiac disease. In this review we synthesize the current understanding of endothelial function and dysfunction as mediators of the cardiomyocyte phenotype in the setting of distinct cardiac pathologies; outline existing in vivo and in vitro models where key features of endothelial cell dysfunction can be recapitulated; and discuss future directions for development of endothelium-targeted therapeutics for cardiac diseases with limited existing treatment options.

Chemokine Fractalkine and Non-Obstructive Coronary Artery Disease—Is There a Link?

“…Endothelium-independent CMD refers to the inability of SMCs to relax despite adequate levels of NO and has similar effects to endothelium-dependent CMD. Damaged endothelium can be characterized by inflammation, changes in permeability or response to vasoactive stimuli [22].…”