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AMPK: Potential Therapeutic Target for Vascular Calcification

Vascular calcification (VC) is an urgent worldwide health issue with no available medical treatment. It is an active cell-driven process by osteogenic differentiation of vascular cells with complex mechanisms. The AMP-activated protein kinase (AMPK) serves as the master sensor of cellular energy sta...

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Autores principales: Lu, Yi, Yuan, Tan, Min, Xinjia, Yuan, Zhen, Cai, Zhejun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8144331/
https://www.ncbi.nlm.nih.gov/pubmed/34046440
http://dx.doi.org/10.3389/fcvm.2021.670222
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author Lu, Yi
Yuan, Tan
Min, Xinjia
Yuan, Zhen
Cai, Zhejun
author_facet Lu, Yi
Yuan, Tan
Min, Xinjia
Yuan, Zhen
Cai, Zhejun
author_sort Lu, Yi
collection PubMed
description Vascular calcification (VC) is an urgent worldwide health issue with no available medical treatment. It is an active cell-driven process by osteogenic differentiation of vascular cells with complex mechanisms. The AMP-activated protein kinase (AMPK) serves as the master sensor of cellular energy status. Accumulating evidence reveals the vital role of AMPK in VC progression. AMPK is involved in VC in various ways, including inhibiting runt-related transcription factor 2 signaling pathways, triggering autophagy, attenuating endoplasmic reticulum stress and dynamic-related protein 1-mediated mitochondrial fission, and activating endothelial nitric oxide synthase. AMPK activators, like metformin, are associated with reduced calcification deposits in certain groups of patients, indicating that AMPK is a potential therapeutic target for VC.
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spelling pubmed-81443312021-05-26 AMPK: Potential Therapeutic Target for Vascular Calcification Lu, Yi Yuan, Tan Min, Xinjia Yuan, Zhen Cai, Zhejun Front Cardiovasc Med Cardiovascular Medicine Vascular calcification (VC) is an urgent worldwide health issue with no available medical treatment. It is an active cell-driven process by osteogenic differentiation of vascular cells with complex mechanisms. The AMP-activated protein kinase (AMPK) serves as the master sensor of cellular energy status. Accumulating evidence reveals the vital role of AMPK in VC progression. AMPK is involved in VC in various ways, including inhibiting runt-related transcription factor 2 signaling pathways, triggering autophagy, attenuating endoplasmic reticulum stress and dynamic-related protein 1-mediated mitochondrial fission, and activating endothelial nitric oxide synthase. AMPK activators, like metformin, are associated with reduced calcification deposits in certain groups of patients, indicating that AMPK is a potential therapeutic target for VC. Frontiers Media S.A. 2021-05-11 /pmc/articles/PMC8144331/ /pubmed/34046440 http://dx.doi.org/10.3389/fcvm.2021.670222 Text en Copyright © 2021 Lu, Yuan, Min, Yuan and Cai. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cardiovascular Medicine
Lu, Yi
Yuan, Tan
Min, Xinjia
Yuan, Zhen
Cai, Zhejun
AMPK: Potential Therapeutic Target for Vascular Calcification
title AMPK: Potential Therapeutic Target for Vascular Calcification
title_full AMPK: Potential Therapeutic Target for Vascular Calcification
title_fullStr AMPK: Potential Therapeutic Target for Vascular Calcification
title_full_unstemmed AMPK: Potential Therapeutic Target for Vascular Calcification
title_short AMPK: Potential Therapeutic Target for Vascular Calcification
title_sort ampk: potential therapeutic target for vascular calcification
topic Cardiovascular Medicine
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8144331/
https://www.ncbi.nlm.nih.gov/pubmed/34046440
http://dx.doi.org/10.3389/fcvm.2021.670222
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