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Antigen-presenting cell-derived extracellular vesicles in accelerating atherosclerosis

Alexander E Berezin 1, * ORCID logo
Alexander A Berezin 2 ORCID logo
  1. Department of Internal Medicine, State Medical University, Zaporozhye, 69035, Ukraine
  2. Department of Internal Medicine, Medical Academy of Post-graduating Education, Zaporozhye, 69000, Ukraine
Correspondence to: Alexander E Berezin, Department of Internal Medicine, State Medical University, Zaporozhye, 69035, Ukraine. ORCID: http://orcid.org/0000-0002-0446-3999. Email: [email protected].
Volume & Issue: Vol. 8 No. 3 (2021) | Page No.: 4258-4266 | DOI: 10.15419/bmrat.v8i3.664
Published: 2021-03-31

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This article is published with open access by BioMedPress. This article is distributed under the terms of the Creative Commons Attribution License (CC-BY 4.0) which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited. 

Abstract

Extracellular vesicles (EVs) are a population of heterogeneous particles that originate from the endosomal system or plasma membrane. Antigen-presenting cells (APCs) produce and release a broad spectrum of EVs involved in the pathogenesis of atherosclerosis. APC-derived EVs contain several bioactive molecules, such as non-coding RNAs, cytokines, chemokines, active proteins, immunomodulatory factors, and growth factors. The review focuses on the role of APC-derived EVs in regulating the transformation of macrophage phenotype, shaping foam cells, driving autophagy and/or inhibiting apoptosis of Th4+ cells, T regulatory cells, endothelial and smooth muscle cells (SMCs), as well as in facilitating oxidative stress in vasculature. APC-derived EVs act as triggers of angiogenesis, neovascularization and inflammation through their participation in microvascular inflammation, angiogenesis, development of atherosclerotic plaques, and modulation of their instability.

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