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The Role of Mitochondria in Vascular Calcification

Vascular calcification (VC) was defined as the ectopic deposition of calcium–phosphorus complexes on the blood vessel walls. It was a process involving multiple factors and mechanisms, covering the phenotype transition of vascular smooth muscle cells (VSMCs) and release of microvesicles. It was a co...

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Detalles Bibliográficos
Autores principales: Wang, Pengbo, Zhang, Naijin, Wu, Boquan, Wu, Shaojun, Zhang, Ying, Sun, Yingxian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Sciendo 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7500121/
https://www.ncbi.nlm.nih.gov/pubmed/32983930
http://dx.doi.org/10.2478/jtim-2020-0013
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author Wang, Pengbo
Zhang, Naijin
Wu, Boquan
Wu, Shaojun
Zhang, Ying
Sun, Yingxian
author_facet Wang, Pengbo
Zhang, Naijin
Wu, Boquan
Wu, Shaojun
Zhang, Ying
Sun, Yingxian
author_sort Wang, Pengbo
collection PubMed
description Vascular calcification (VC) was defined as the ectopic deposition of calcium–phosphorus complexes on the blood vessel walls. It was a process involving multiple factors and mechanisms, covering the phenotype transition of vascular smooth muscle cells (VSMCs) and release of microvesicles. It was a common end-stage alteration of chronic diseases such as cardiovascular disease and chronic kidney disease. Increasing evidence indicates that mitochondria were involved in the development of VC. Mitochondria provided energy to cells, maintained the stability of cell functions, and participated in a variety of biological behavior. Oxidative stress, autophagy, apoptosis, and mitochondrial DNA (mtDNA) damage could affect the development of VSMCs calcification by alteration of mitochondrial function. This article reviewed the mechanism of calcification and the role of mitochondria in VC, aiming to raise a novel insight into drug development and clinical treatment.
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spelling pubmed-75001212020-09-25 The Role of Mitochondria in Vascular Calcification Wang, Pengbo Zhang, Naijin Wu, Boquan Wu, Shaojun Zhang, Ying Sun, Yingxian J Transl Int Med Review Article Vascular calcification (VC) was defined as the ectopic deposition of calcium–phosphorus complexes on the blood vessel walls. It was a process involving multiple factors and mechanisms, covering the phenotype transition of vascular smooth muscle cells (VSMCs) and release of microvesicles. It was a common end-stage alteration of chronic diseases such as cardiovascular disease and chronic kidney disease. Increasing evidence indicates that mitochondria were involved in the development of VC. Mitochondria provided energy to cells, maintained the stability of cell functions, and participated in a variety of biological behavior. Oxidative stress, autophagy, apoptosis, and mitochondrial DNA (mtDNA) damage could affect the development of VSMCs calcification by alteration of mitochondrial function. This article reviewed the mechanism of calcification and the role of mitochondria in VC, aiming to raise a novel insight into drug development and clinical treatment. Sciendo 2020-06-30 /pmc/articles/PMC7500121/ /pubmed/32983930 http://dx.doi.org/10.2478/jtim-2020-0013 Text en © 2020 Pengbo Wang et al., published by Sciendo http://creativecommons.org/licenses/by-nc-nd/4.0 This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
spellingShingle Review Article
Wang, Pengbo
Zhang, Naijin
Wu, Boquan
Wu, Shaojun
Zhang, Ying
Sun, Yingxian
The Role of Mitochondria in Vascular Calcification
title The Role of Mitochondria in Vascular Calcification
title_full The Role of Mitochondria in Vascular Calcification
title_fullStr The Role of Mitochondria in Vascular Calcification
title_full_unstemmed The Role of Mitochondria in Vascular Calcification
title_short The Role of Mitochondria in Vascular Calcification
title_sort role of mitochondria in vascular calcification
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7500121/
https://www.ncbi.nlm.nih.gov/pubmed/32983930
http://dx.doi.org/10.2478/jtim-2020-0013
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