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Aging Triggers Mitochondrial Dysfunction in Mice
Direct analysis of isolated mitochondria from old mice enables a better understanding of heart senescence dysfunction. Despite a well-defined senescent phenotype in cardiomyocytes, the mitochondrial state in aged cardiomyocytes is still unclear. Here, we report data about mitochondrial function in o...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10342046/ https://www.ncbi.nlm.nih.gov/pubmed/37445770 http://dx.doi.org/10.3390/ijms241310591 |
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author | Rosa, Frederico Luis Lima de Souza, Itanna Isis Araujo Monnerat, Gustavo Campos de Carvalho, Antonio Carlos Maciel, Leonardo |
author_facet | Rosa, Frederico Luis Lima de Souza, Itanna Isis Araujo Monnerat, Gustavo Campos de Carvalho, Antonio Carlos Maciel, Leonardo |
author_sort | Rosa, Frederico Luis Lima |
collection | PubMed |
description | Direct analysis of isolated mitochondria from old mice enables a better understanding of heart senescence dysfunction. Despite a well-defined senescent phenotype in cardiomyocytes, the mitochondrial state in aged cardiomyocytes is still unclear. Here, we report data about mitochondrial function in old mice. Isolated cardiomyocytes’ mitochondria were obtained by differential centrifugation from old and young mice hearts to perform functional analyses of mitochondrial O(2) consumption, transmembrane potential, ROS formation, ATP production, and swelling. Our results show that mitochondria from old mouse hearts have reduced oxygen consumption during the phosphorylative states of complexes I and II. Additionally, these mitochondria produced more ROS and less ATP than those of young hearts. Mitochondria from old hearts also showed a depolarized membrane potential than mitochondria from young hearts and, as expected, a greater electron leak. Our results indicate that mitochondria from senescent cardiomyocytes are less efficient in O(2) consumption, generating more ROS and producing less ATP. Furthermore, the phosphorylative state of complexes I and II presents a functional defect, contributing to greater leakage of protons and ROS production that can be harmful to the cell. |
format | Online Article Text |
id | pubmed-10342046 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-103420462023-07-14 Aging Triggers Mitochondrial Dysfunction in Mice Rosa, Frederico Luis Lima de Souza, Itanna Isis Araujo Monnerat, Gustavo Campos de Carvalho, Antonio Carlos Maciel, Leonardo Int J Mol Sci Communication Direct analysis of isolated mitochondria from old mice enables a better understanding of heart senescence dysfunction. Despite a well-defined senescent phenotype in cardiomyocytes, the mitochondrial state in aged cardiomyocytes is still unclear. Here, we report data about mitochondrial function in old mice. Isolated cardiomyocytes’ mitochondria were obtained by differential centrifugation from old and young mice hearts to perform functional analyses of mitochondrial O(2) consumption, transmembrane potential, ROS formation, ATP production, and swelling. Our results show that mitochondria from old mouse hearts have reduced oxygen consumption during the phosphorylative states of complexes I and II. Additionally, these mitochondria produced more ROS and less ATP than those of young hearts. Mitochondria from old hearts also showed a depolarized membrane potential than mitochondria from young hearts and, as expected, a greater electron leak. Our results indicate that mitochondria from senescent cardiomyocytes are less efficient in O(2) consumption, generating more ROS and producing less ATP. Furthermore, the phosphorylative state of complexes I and II presents a functional defect, contributing to greater leakage of protons and ROS production that can be harmful to the cell. MDPI 2023-06-24 /pmc/articles/PMC10342046/ /pubmed/37445770 http://dx.doi.org/10.3390/ijms241310591 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/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 (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Communication Rosa, Frederico Luis Lima de Souza, Itanna Isis Araujo Monnerat, Gustavo Campos de Carvalho, Antonio Carlos Maciel, Leonardo Aging Triggers Mitochondrial Dysfunction in Mice |
title | Aging Triggers Mitochondrial Dysfunction in Mice |
title_full | Aging Triggers Mitochondrial Dysfunction in Mice |
title_fullStr | Aging Triggers Mitochondrial Dysfunction in Mice |
title_full_unstemmed | Aging Triggers Mitochondrial Dysfunction in Mice |
title_short | Aging Triggers Mitochondrial Dysfunction in Mice |
title_sort | aging triggers mitochondrial dysfunction in mice |
topic | Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10342046/ https://www.ncbi.nlm.nih.gov/pubmed/37445770 http://dx.doi.org/10.3390/ijms241310591 |
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