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Mitochondrial Quality Control in the Heart: New Drug Targets for Cardiovascular Disease

Despite considerable efforts to prevent and treat cardiovascular disease (CVD), it has become the leading cause of death worldwide. Cardiac mitochondria are crucial cell organelles responsible for creating energy-rich ATP and mitochondrial dysfunction is the root cause for developing heart failure....

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Autores principales: Oh, Chang-Myung, Ryu, Dongryeol, Cho, Sungsoo, Jang, Yangsoo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society of Cardiology 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7098821/
https://www.ncbi.nlm.nih.gov/pubmed/32216174
http://dx.doi.org/10.4070/kcj.2019.0416
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author Oh, Chang-Myung
Ryu, Dongryeol
Cho, Sungsoo
Jang, Yangsoo
author_facet Oh, Chang-Myung
Ryu, Dongryeol
Cho, Sungsoo
Jang, Yangsoo
author_sort Oh, Chang-Myung
collection PubMed
description Despite considerable efforts to prevent and treat cardiovascular disease (CVD), it has become the leading cause of death worldwide. Cardiac mitochondria are crucial cell organelles responsible for creating energy-rich ATP and mitochondrial dysfunction is the root cause for developing heart failure. Therefore, maintenance of mitochondrial quality control (MQC) is an essential process for cardiovascular homeostasis and cardiac health. In this review, we describe the major mechanisms of MQC system, such as mitochondrial unfolded protein response and mitophagy. Moreover, we describe the results of MQC failure in cardiac mitochondria. Furthermore, we discuss the prospects of 2 drug candidates, urolithin A and spermidine, for restoring mitochondrial homeostasis to treat CVD.
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spelling pubmed-70988212020-05-01 Mitochondrial Quality Control in the Heart: New Drug Targets for Cardiovascular Disease Oh, Chang-Myung Ryu, Dongryeol Cho, Sungsoo Jang, Yangsoo Korean Circ J Review Article Despite considerable efforts to prevent and treat cardiovascular disease (CVD), it has become the leading cause of death worldwide. Cardiac mitochondria are crucial cell organelles responsible for creating energy-rich ATP and mitochondrial dysfunction is the root cause for developing heart failure. Therefore, maintenance of mitochondrial quality control (MQC) is an essential process for cardiovascular homeostasis and cardiac health. In this review, we describe the major mechanisms of MQC system, such as mitochondrial unfolded protein response and mitophagy. Moreover, we describe the results of MQC failure in cardiac mitochondria. Furthermore, we discuss the prospects of 2 drug candidates, urolithin A and spermidine, for restoring mitochondrial homeostasis to treat CVD. The Korean Society of Cardiology 2020-03-09 /pmc/articles/PMC7098821/ /pubmed/32216174 http://dx.doi.org/10.4070/kcj.2019.0416 Text en Copyright © 2020. The Korean Society of Cardiology https://creativecommons.org/licenses/by-nc/4.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Oh, Chang-Myung
Ryu, Dongryeol
Cho, Sungsoo
Jang, Yangsoo
Mitochondrial Quality Control in the Heart: New Drug Targets for Cardiovascular Disease
title Mitochondrial Quality Control in the Heart: New Drug Targets for Cardiovascular Disease
title_full Mitochondrial Quality Control in the Heart: New Drug Targets for Cardiovascular Disease
title_fullStr Mitochondrial Quality Control in the Heart: New Drug Targets for Cardiovascular Disease
title_full_unstemmed Mitochondrial Quality Control in the Heart: New Drug Targets for Cardiovascular Disease
title_short Mitochondrial Quality Control in the Heart: New Drug Targets for Cardiovascular Disease
title_sort mitochondrial quality control in the heart: new drug targets for cardiovascular disease
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7098821/
https://www.ncbi.nlm.nih.gov/pubmed/32216174
http://dx.doi.org/10.4070/kcj.2019.0416
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