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Atherosclerosis and Coenzyme Q(10)

Atherosclerosis is the most common cause of cardiac deaths worldwide. Classically, atherosclerosis has been explained as a simple arterial lipid deposition with concomitant loss of vascular elasticity. Eventually, this condition can lead to consequent blood flow reduction through the affected vessel...

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Autores principales: Suárez-Rivero, Juan M., Pastor-Maldonado, Carmen J., de la Mata, Mario, Villanueva-Paz, Marina, Povea-Cabello, Suleva, Álvarez-Córdoba, Mónica, Villalón-García, Irene, Suárez-Carrillo, Alejandra, Talaverón-Rey, Marta, Munuera, Manuel, Sánchez-Alcázar, José A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6834161/
https://www.ncbi.nlm.nih.gov/pubmed/31635164
http://dx.doi.org/10.3390/ijms20205195
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author Suárez-Rivero, Juan M.
Pastor-Maldonado, Carmen J.
de la Mata, Mario
Villanueva-Paz, Marina
Povea-Cabello, Suleva
Álvarez-Córdoba, Mónica
Villalón-García, Irene
Suárez-Carrillo, Alejandra
Talaverón-Rey, Marta
Munuera, Manuel
Sánchez-Alcázar, José A.
author_facet Suárez-Rivero, Juan M.
Pastor-Maldonado, Carmen J.
de la Mata, Mario
Villanueva-Paz, Marina
Povea-Cabello, Suleva
Álvarez-Córdoba, Mónica
Villalón-García, Irene
Suárez-Carrillo, Alejandra
Talaverón-Rey, Marta
Munuera, Manuel
Sánchez-Alcázar, José A.
author_sort Suárez-Rivero, Juan M.
collection PubMed
description Atherosclerosis is the most common cause of cardiac deaths worldwide. Classically, atherosclerosis has been explained as a simple arterial lipid deposition with concomitant loss of vascular elasticity. Eventually, this condition can lead to consequent blood flow reduction through the affected vessel. However, numerous studies have demonstrated that more factors than lipid accumulation are involved in arterial damage at the cellular level, such as inflammation, autophagy impairment, mitochondrial dysfunction, and/or free-radical overproduction. In order to consider the correction of all of these pathological changes, new approaches in atherosclerosis treatment are necessary. Ubiquinone or coenzyme Q(10) is a multifunctional molecule that could theoretically revert most of the cellular alterations found in atherosclerosis, such as cholesterol biosynthesis dysregulation, impaired autophagy flux and mitochondrial dysfunction thanks to its redox and signaling properties. In this review, we will show the latest advances in the knowledge of the relationships between coenzyme Q(10) and atherosclerosis. In addition, as atherosclerosis phenotype is closely related to aging, it is reasonable to believe that coenzyme Q(10) supplementation could be beneficial for both conditions.
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spelling pubmed-68341612019-11-25 Atherosclerosis and Coenzyme Q(10) Suárez-Rivero, Juan M. Pastor-Maldonado, Carmen J. de la Mata, Mario Villanueva-Paz, Marina Povea-Cabello, Suleva Álvarez-Córdoba, Mónica Villalón-García, Irene Suárez-Carrillo, Alejandra Talaverón-Rey, Marta Munuera, Manuel Sánchez-Alcázar, José A. Int J Mol Sci Review Atherosclerosis is the most common cause of cardiac deaths worldwide. Classically, atherosclerosis has been explained as a simple arterial lipid deposition with concomitant loss of vascular elasticity. Eventually, this condition can lead to consequent blood flow reduction through the affected vessel. However, numerous studies have demonstrated that more factors than lipid accumulation are involved in arterial damage at the cellular level, such as inflammation, autophagy impairment, mitochondrial dysfunction, and/or free-radical overproduction. In order to consider the correction of all of these pathological changes, new approaches in atherosclerosis treatment are necessary. Ubiquinone or coenzyme Q(10) is a multifunctional molecule that could theoretically revert most of the cellular alterations found in atherosclerosis, such as cholesterol biosynthesis dysregulation, impaired autophagy flux and mitochondrial dysfunction thanks to its redox and signaling properties. In this review, we will show the latest advances in the knowledge of the relationships between coenzyme Q(10) and atherosclerosis. In addition, as atherosclerosis phenotype is closely related to aging, it is reasonable to believe that coenzyme Q(10) supplementation could be beneficial for both conditions. MDPI 2019-10-20 /pmc/articles/PMC6834161/ /pubmed/31635164 http://dx.doi.org/10.3390/ijms20205195 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Suárez-Rivero, Juan M.
Pastor-Maldonado, Carmen J.
de la Mata, Mario
Villanueva-Paz, Marina
Povea-Cabello, Suleva
Álvarez-Córdoba, Mónica
Villalón-García, Irene
Suárez-Carrillo, Alejandra
Talaverón-Rey, Marta
Munuera, Manuel
Sánchez-Alcázar, José A.
Atherosclerosis and Coenzyme Q(10)
title Atherosclerosis and Coenzyme Q(10)
title_full Atherosclerosis and Coenzyme Q(10)
title_fullStr Atherosclerosis and Coenzyme Q(10)
title_full_unstemmed Atherosclerosis and Coenzyme Q(10)
title_short Atherosclerosis and Coenzyme Q(10)
title_sort atherosclerosis and coenzyme q(10)
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6834161/
https://www.ncbi.nlm.nih.gov/pubmed/31635164
http://dx.doi.org/10.3390/ijms20205195
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