The role of mitochondria in the development of cardiovascular diseases

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Abstract

INTRODUCTION: A large amount of experimental and clinical data has been accumulated that evidence the involvement of cardiomyocyte mitochondria in the pathogenesis of heart failure, cardiomyopathies and ischemic-reperfusion myocardial injury. Morphological changes of cardiomyocyte mitochondria include hyperplasia, decreased organelle size and broken structural integrity. Overexpression of various microRNAs suppresses mRNA transcription and the activity of enzymes and proteins involved in β-oxidation of fatty acids, Krebs cycle functioning, ATP production. It also inhibits the expression of genes regulating adaptive and maladaptive cardiac remodeling in heart failure. All the above events are accompanied by decreased ATP synthesis, release of pro-apoptotic proteins, fibrosis and cardiac hypertrophy.

AIM: To analyze and systematize modern data on the role of mitochondrial dysfunction in the pathogenesis of cardiovascular diseases, and potential ways of its correction.

To find material for this review article, we used the abstracting databases PubMed, Google Scholar, and eLibrary. The search included publications from 2013 to 2023.

Analysis of literature sources showed that mitochondrial dysfunction has recently been considered an important factor in the development of heart failure. It also revealed the relationship between cardiomyopathies and mitochondrial failure as well as its role as a critical pathophysiological factor of myocardial destruction in ischemia/reperfusion. Additionally, data were obtained about an ambiguous role of microRNA-dependent regulation of the mitochondrial genes and their involvement in the development of cardiovascular diseases. Of importance is search for mitochondria-targeted medical drugs for the treatment of cardiovascular diseases. The promising drug targets are reactive oxygen species, factors controlling mitochondrial fission and fusion, biogenesis and autophagy, modulators of mitochondrial microRNA expression, and mitochondrial permeability pores.

CONCLUSION: Cardiovascular diseases induced by mitochondrial dysfunction, can be associated with different organelle damages. New technologies of investigating molecular mechanisms underlying mitochondrial dysfunction and precise understanding of these disorders open up opportunities to more clearly define pathophysiological aspects and develop new therapeutic approaches for the treatment of circulatory diseases.

About the authors

Hala Deeb

Al Hawash Private University

Email: hala197944@gmail.com
ORCID iD: 0009-0008-8878-0529

PhD (in Biology), Assistant Professor

Syrian Arab Republic, Homs

Valentina N. Perfilova

Volgograd State Medical University

Author for correspondence.
Email: vnperfilova@mail.ru
ORCID iD: 0000-0002-2457-8486
SPIN-code: 3291-9904

Dr. Sci. (Biology), Professor

Russian Federation, Volgograd

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