Important determinants of endothelial homeostasis include not only endothelial membrane function and adhesiveness to proteins of the coagulation cascade and platelets but also membrane permeability and the integrity, that is, endovascular coverage by ECs ( 30). In the mid and long term, changes in endothelial homeostasis ( i.e., endothelial injury) affect the vascular structure by interacting with extracellular matrix turnover and smooth muscle cells controlling intimal hyperplasia. Endothelial homeostasis encompasses a number of acute responses such as adaption of flow to tissue's demand via mechanosensing and acute modulation of vascular tone via production of autocoids, including nitric oxide (NO), that are affected by sympathetic tone ( Fig. This article aims at capturing current knowledge on the role of endothelial homeostasis, maintenance of endothelial integrity, and functional competence throughout life. 22, 1230–1242.Ī disturbance of endothelial function is considered a key event in the development and progression of atherosclerosis ( 94).
Future Directions: Endothelial homeostasis may be a clinical therapeutic target for cardiovascular health maintenance. Critical Issues: Improvements of reproducibility and observer independence of FMD measurements and definitions of relevant EMP and CAC subpopulations warrant further research. These markers can be integrated in a clinical endothelial phenotype, reflecting the net result between damage from risk factors and endogenous repair capacity with NO representing a central signaling molecule.
Flow-mediated vasodilation (FMD) is a generally accepted clinical read-out of NO-dependent vasodilation, whereas EMP are upcoming prognostically validated markers of endothelial injury and CAC are reflective of the regenerative capacity with both expressing a functional eNOS. The balance and the intensity of endothelial damage and repair might be reflected by changes in circulating endothelial microparticles (EMP) and CAC. Recent Advances: Endothelial homeostasis encompasses acute responses such as adaption of flow to tissue's demand and more sustained responses to injury such as re-endothelialization and sprouting of endothelial cells (ECs) and attraction of circulating angiogenic cells (CAC), both of which support repair of damaged endothelium.
Endothelial nitric oxide synthase (eNOS) is a central regulator of cellular function that is important to maintain endothelial homeostasis. Significance: Disruption of endothelial function is considered a key event in the development and progression of atherosclerosis.
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