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Cellular and humoral mechanisms of interstitial myocardial fibrosis

Authors: Khugaev G.A.

Company: Bakoulev National Medical Research Center for Cardiovascular Surgery, Moscow, Russian Federation

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Type:  Reviews


DOI: https://doi.org/10.24022/1997-3187-2022-16-4-470-482

For citation: Khugaev G.A. Cellular and humoral mechanisms of interstitial myocardial fibrosis. Creative Cardiology. 2022; 16 (4): 470–82 (in Russ.). DOI: 10.24022/1997-3187-2022-16-4-470-482

Received / Accepted:  27.06.2022 / 07.12.2022

Keywords: interstitial myocardial fibrosis left ventricle fibroblasts myofibroblasts myocardial pressure overload

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Abstract

Interstitial myocardial fibrosis is a typical pathological process associated with various cardiovascular diseases, which is an increasing interstitial space in myocardium as a result of excessive accumulation of interstitial cells and extracellular matter in it. The most common cause of interstitial fibrosis is myocardial pressure overload. All known types of myocardial cells participate in the development of fibrosis, both interstitial (fibroblasts, myofibroblasts, immune cells, pericytes, endothelial cells, telocytes) and cardiomyocytes. The main mechanism of myocardial fibrosis is the activation of resident fibroblasts and their transformation into myofibroblasts, which are the main producers of both stromal and matricellular proteins. Immune cells, pericytes, endothelial cells, telocytes and cardiomyocytes activate fibroblasts through signaling of mediators such as growth factors (transforming growth factor β, platelet growth factor) and cytokines (tumor necrosis factor α, interleukin 1, 4, 6, and 10). In addition, fibroblasts can directly perceive mechanical stress with the participation of mechanosensitive receptors, ion channels and integrin proteins. Prolonged pressure overload leads to a change in the balance of matrix metalloproteinases and their inhibitors, dilation of the left ventricle and systolic dysfunction.

This review article discusses the mechanisms of interstitial myocardial fibrosis with special attention to the interaction of interstitial cells and cardiomyocytes.

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About Authors

Georgiy A. Khugaev, Junior Researcher, Assistant of the Chair; ORCID

Chief Editor

Leo A. Bockeria, MD, PhD, DSc, Professor, Academician of Russian Academy of Sciences, President of Bakoulev National Medical Research Center for Cardiovascular Surgery


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