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Mitochondria and Calcium Homeostasis: Cisd2 as a Big Player in Cardiac Ageing
The ageing of human populations has become a problem throughout the world. In this context, increasing the healthy lifespan of individuals has become an important target for medical research and governments. Cardiac disease remains the leading cause of morbidity and mortality in ageing populations a...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7731030/ https://www.ncbi.nlm.nih.gov/pubmed/33287440 http://dx.doi.org/10.3390/ijms21239238 |
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author | Yeh, Chi-Hsiao Chou, Yi-Ju Kao, Cheng-Heng Tsai, Ting-Fen |
author_facet | Yeh, Chi-Hsiao Chou, Yi-Ju Kao, Cheng-Heng Tsai, Ting-Fen |
author_sort | Yeh, Chi-Hsiao |
collection | PubMed |
description | The ageing of human populations has become a problem throughout the world. In this context, increasing the healthy lifespan of individuals has become an important target for medical research and governments. Cardiac disease remains the leading cause of morbidity and mortality in ageing populations and results in significant increases in healthcare costs. Although clinical and basic research have revealed many novel insights into the pathways that drive heart failure, the molecular mechanisms underlying cardiac ageing and age-related cardiac dysfunction are still not fully understood. In this review we summarize the most updated publications and discuss the central components that drive cardiac ageing. The following characters of mitochondria-related dysfunction have been identified during cardiac ageing: (a) disruption of the integrity of mitochondria-associated membrane (MAM) contact sites; (b) dysregulation of energy metabolism and dynamic flexibility; (c) dyshomeostasis of Ca(2+) control; (d) disturbance to mitochondria–lysosomal crosstalk. Furthermore, Cisd2, a pro-longevity gene, is known to be mainly located in the endoplasmic reticulum (ER), mitochondria, and MAM. The expression level of Cisd2 decreases during cardiac ageing. Remarkably, a high level of Cisd2 delays cardiac ageing and ameliorates age-related cardiac dysfunction; this occurs by maintaining correct regulation of energy metabolism and allowing dynamic control of metabolic flexibility. Together, our previous studies and new evidence provided here highlight Cisd2 as a novel target for developing therapies to promote healthy ageing |
format | Online Article Text |
id | pubmed-7731030 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-77310302020-12-12 Mitochondria and Calcium Homeostasis: Cisd2 as a Big Player in Cardiac Ageing Yeh, Chi-Hsiao Chou, Yi-Ju Kao, Cheng-Heng Tsai, Ting-Fen Int J Mol Sci Review The ageing of human populations has become a problem throughout the world. In this context, increasing the healthy lifespan of individuals has become an important target for medical research and governments. Cardiac disease remains the leading cause of morbidity and mortality in ageing populations and results in significant increases in healthcare costs. Although clinical and basic research have revealed many novel insights into the pathways that drive heart failure, the molecular mechanisms underlying cardiac ageing and age-related cardiac dysfunction are still not fully understood. In this review we summarize the most updated publications and discuss the central components that drive cardiac ageing. The following characters of mitochondria-related dysfunction have been identified during cardiac ageing: (a) disruption of the integrity of mitochondria-associated membrane (MAM) contact sites; (b) dysregulation of energy metabolism and dynamic flexibility; (c) dyshomeostasis of Ca(2+) control; (d) disturbance to mitochondria–lysosomal crosstalk. Furthermore, Cisd2, a pro-longevity gene, is known to be mainly located in the endoplasmic reticulum (ER), mitochondria, and MAM. The expression level of Cisd2 decreases during cardiac ageing. Remarkably, a high level of Cisd2 delays cardiac ageing and ameliorates age-related cardiac dysfunction; this occurs by maintaining correct regulation of energy metabolism and allowing dynamic control of metabolic flexibility. Together, our previous studies and new evidence provided here highlight Cisd2 as a novel target for developing therapies to promote healthy ageing MDPI 2020-12-03 /pmc/articles/PMC7731030/ /pubmed/33287440 http://dx.doi.org/10.3390/ijms21239238 Text en © 2020 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 Yeh, Chi-Hsiao Chou, Yi-Ju Kao, Cheng-Heng Tsai, Ting-Fen Mitochondria and Calcium Homeostasis: Cisd2 as a Big Player in Cardiac Ageing |
title | Mitochondria and Calcium Homeostasis: Cisd2 as a Big Player in Cardiac Ageing |
title_full | Mitochondria and Calcium Homeostasis: Cisd2 as a Big Player in Cardiac Ageing |
title_fullStr | Mitochondria and Calcium Homeostasis: Cisd2 as a Big Player in Cardiac Ageing |
title_full_unstemmed | Mitochondria and Calcium Homeostasis: Cisd2 as a Big Player in Cardiac Ageing |
title_short | Mitochondria and Calcium Homeostasis: Cisd2 as a Big Player in Cardiac Ageing |
title_sort | mitochondria and calcium homeostasis: cisd2 as a big player in cardiac ageing |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7731030/ https://www.ncbi.nlm.nih.gov/pubmed/33287440 http://dx.doi.org/10.3390/ijms21239238 |
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