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Molecular and Cellular Aspects of the Endothelial–Mesenchymal Transition in Cardiovascular Diseases

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Abstract

Endothelial cells (ECs), which form the inner surface of the blood vessels, contact the blood, withstand mechanical pressure, and demonstrate heterogeneous reactions to exogenous and endogenous stimuli. ECs have unique properties in accordance with their niches and play an important role in regulating vascular homeostasis. Endothelial cells may undergo a dynamic phenotypic switch in terms of its heterogeneity, which may lead to endothelial dysfunction and a number of associated pathologies. Endothelial–mesenchymal transition (EndMT) is one of the possible molecular and cellular mechanisms of this kind. EndMT is characterized by phenotypic changes in ECs through which endothelial cells acquire new properties, i.e., start producing mesenchymal markers such as alpha-SMA and vimentin, change morphology, and become able to migrate. EndMT is a complex biological process that can be induced by inflammation, hypoxia, or oxidative stress and be involved in pathogenesis of cardiovascular disease. This review describes the key markers, inhibitors, and inducers of endothelial–mesenchymal transition and overall state-of-the-art of EndMT in cardiovascular diseases.

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  1. Pavlov Ryazan State Medical University, Ministry of Health of the Russian Federation, 390026, Ryazan, Russia

    E. A. Strelnikova, R. E. Kalinin, I. A. Suchkov, N. V. Korotkova & N. D. Mzhavanadze

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  1. E. A. Strelnikova
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  2. R. E. Kalinin
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Translated by M. Batrukova

Abbreviations: SMC, smooth muscle cells; RT-PCR, real-time reverse transcription polymerase chain reaction; EC, endothelial cells; BMP, bone morphogenetic protein; EMT, epithelial-to-mesenchymal transition; EndMT, endothelial–mesenchymal transition; EPCR, endothelial cell protein C receptor; FGF, fibroblast growth factor; ICAM-1, intercellular adhesion molecule 1; IL, interleukin; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; PAI-1, plasminogen activator inhibitor-1; PECAM-1, platelet endothelial cell adhesion molecule; SM22α, smooth muscle 22α; TGF-β, transforming growth factor-β; TNF-α, tumor necrosis factor α; VCAM-1, vascular cell adhesion molecule 1; α-SMA, α-smooth muscle actin.

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Strelnikova, E.A., Kalinin, R.E., Suchkov, I.A. et al. Molecular and Cellular Aspects of the Endothelial–Mesenchymal Transition in Cardiovascular Diseases. Mol Biol 57, 563–571 (2023). https://doi.org/10.1134/S0026893323030111

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