The endothelium, as the innermost layer of the vessel wall, exhibits selective permeability to many biologically active substances and blood cells, and has a direct effect on the adjacent tissues. With the participation of biochemical and humoral factors, a cascade of proinflammatory and prothrombotic changes is induced, leading to endothelial dysfunction, associated with the loss of barrier function, the production of reactive oxygen species by cells, the alteration of histoarchitectonics of organs, and, as a result, the development of cardiovascular diseases.
OBJECTIVE
To analyze modern views and concepts of pathophysiological and morphological mechanisms of endothelial dysfunction development and its impact on the occurrence and course of cardiovascular diseases.
MATERIALS AND METHODS
The scientific literature and articles published over the past decade were searched and analyzed using the PubMed and eLibrary search engines for the following keywords: «endothelium», «endothelial dysfunction», and «cardiovascular diseases».
RESULTS
The endothelium, due to the production of nitric oxide, is involved in the regulation of blood vessel tone, and the synthesis of angiotensin-II, endothelin-1, neuregulin-1, and apelin maintains homeostasis of the heart muscle. Humoral and biochemical triggers, such as angiotensin-II, proinflammatory cytokines, and oxidative stress, induce dystrophic changes in the vascular wall, leading to the activation of the endothelium, altering secretion of the above biologically active substances with the development of systemic vascular inflammation, contributing to vascular remodeling, increased stiffness, and reducing the perfusion of the heart muscle. In response to endothelial dysfunction and chronic myocardial ischemia, fibrosis, cardiomyocyte proliferation, and vicarious hypertrophy occur, which are predictors of cardiovascular pathology.
CONCLUSION
The analysis of scientific data of the last decade proves the effect of endothelial dysfunction on the course of cardiovascular disorders, such as coronary microvascular dysfunction, coronary heart disease, hypertrophic cardiomyopathy, and heart failure. However, the search for therapeutic, including medicinal, approaches to modify this link in the pathological process is still relevant.
