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Assessment of endothelial apoptosis in the pulmonary arteries of rats with monocrotaline-induced pulmonary arterial hypertension

https://doi.org/10.58708/2074-2088.2024-2(32)-37-43

Abstract

Pulmonary arterial hypertension (PAH) is a severe, rapidly progressing disease. Apoptosis of endothelial cells (EC) and their resistance to programmed death play a decisive role in the pathogenesis of PAH. It is assumed that the ratio of Bcl-2 and Bax proteins may be the main determinant of cellular ability to apoptosis. The article presents the results of a study of pulmonary artery EC apoptosis in the dynamics of monocrotaline-induced PAH development.
Apoptosis is an important factor in arterial remodeling in PAH. With the development of PAH, activation of apoptotic death of EC reaches its maximum values 1 month after the beginning of the experiment; 2 months after the introduction of monocrotaline (MCT) to rats, apoptosis transitions to necrosis and a decrease in the apoptotic index is observed.
Inhibition of anti-apoptotic mechanisms in the early stages of PAH leads to impaired permeability of the EC barrier and the risk of thrombosis. Apoptosis of EC is characterized by a decrease in the expression of the anti-apoptotic factor Bcl-2 with a fairly high expression value of the pro-apoptotic protein Baх.
Thus, the ratio of pro- and anti-apoptotic proteins of the Bcl-2 family plays a significant role in the development of pathological changes in the pulmonary arteries in rats with PAH.

About the Authors

T. Ye. Vladimirskaja
Белорусский государственный медицинский университет
Belarus


I. Ye. Adzeriho
Белорусский государственный медицинский университет
Belarus


A. M. Ustemchuk
Белорусский государственный медицинский университет
Belarus


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For citations:


Vladimirskaja T.Ye., Adzeriho I.Ye., Ustemchuk A.M. Assessment of endothelial apoptosis in the pulmonary arteries of rats with monocrotaline-induced pulmonary arterial hypertension. Medical and Biological Problems of Life Activity. 2024;(2):37-43. (In Russ.) https://doi.org/10.58708/2074-2088.2024-2(32)-37-43

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ISSN 2074-2088 (Print)