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Selective Cardiomyocyte Oxidative Stress Leads to Bystander Senescence of Cardiac Stromal Cells
Accumulation of senescent cells in tissues during normal or accelerated aging has been shown to be detrimental and to favor the outcomes of age-related diseases such as heart failure (HF). We have previously shown that oxidative stress dependent on monoamine oxidase A (MAOA) activity in cardiomyocyt...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7956294/ https://www.ncbi.nlm.nih.gov/pubmed/33668142 http://dx.doi.org/10.3390/ijms22052245 |
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author | Martini, Hélène Lefevre, Lise Sayir, Sylvain Itier, Romain Maggiorani, Damien Dutaur, Marianne Marsal, Dimitri J. Roncalli, Jérôme Pizzinat, Nathalie Cussac, Daniel Parini, Angelo Mialet-Perez, Jeanne Douin-Echinard, Victorine |
author_facet | Martini, Hélène Lefevre, Lise Sayir, Sylvain Itier, Romain Maggiorani, Damien Dutaur, Marianne Marsal, Dimitri J. Roncalli, Jérôme Pizzinat, Nathalie Cussac, Daniel Parini, Angelo Mialet-Perez, Jeanne Douin-Echinard, Victorine |
author_sort | Martini, Hélène |
collection | PubMed |
description | Accumulation of senescent cells in tissues during normal or accelerated aging has been shown to be detrimental and to favor the outcomes of age-related diseases such as heart failure (HF). We have previously shown that oxidative stress dependent on monoamine oxidase A (MAOA) activity in cardiomyocytes promotes mitochondrial damage, the formation of telomere-associated foci, senescence markers, and triggers systolic cardiac dysfunction in a model of transgenic mice overexpressing MAOA in cardiomyocytes (Tg MAOA). However, the impact of cardiomyocyte oxidative stress on the cardiac microenvironment in vivo is still unclear. Our results showed that systolic cardiac dysfunction in Tg MAOA mice was strongly correlated with oxidative stress induced premature senescence of cardiac stromal cells favoring the recruitment of CCR2(+) monocytes and the installation of cardiac inflammation. Understanding the interplay between oxidative stress induced premature senescence and accelerated cardiac dysfunction will help to define new molecular pathways at the crossroad between cardiac dysfunction and accelerated aging, which could contribute to the increased susceptibility of the elderly to HF. |
format | Online Article Text |
id | pubmed-7956294 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-79562942021-03-15 Selective Cardiomyocyte Oxidative Stress Leads to Bystander Senescence of Cardiac Stromal Cells Martini, Hélène Lefevre, Lise Sayir, Sylvain Itier, Romain Maggiorani, Damien Dutaur, Marianne Marsal, Dimitri J. Roncalli, Jérôme Pizzinat, Nathalie Cussac, Daniel Parini, Angelo Mialet-Perez, Jeanne Douin-Echinard, Victorine Int J Mol Sci Article Accumulation of senescent cells in tissues during normal or accelerated aging has been shown to be detrimental and to favor the outcomes of age-related diseases such as heart failure (HF). We have previously shown that oxidative stress dependent on monoamine oxidase A (MAOA) activity in cardiomyocytes promotes mitochondrial damage, the formation of telomere-associated foci, senescence markers, and triggers systolic cardiac dysfunction in a model of transgenic mice overexpressing MAOA in cardiomyocytes (Tg MAOA). However, the impact of cardiomyocyte oxidative stress on the cardiac microenvironment in vivo is still unclear. Our results showed that systolic cardiac dysfunction in Tg MAOA mice was strongly correlated with oxidative stress induced premature senescence of cardiac stromal cells favoring the recruitment of CCR2(+) monocytes and the installation of cardiac inflammation. Understanding the interplay between oxidative stress induced premature senescence and accelerated cardiac dysfunction will help to define new molecular pathways at the crossroad between cardiac dysfunction and accelerated aging, which could contribute to the increased susceptibility of the elderly to HF. MDPI 2021-02-24 /pmc/articles/PMC7956294/ /pubmed/33668142 http://dx.doi.org/10.3390/ijms22052245 Text en © 2021 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 | Article Martini, Hélène Lefevre, Lise Sayir, Sylvain Itier, Romain Maggiorani, Damien Dutaur, Marianne Marsal, Dimitri J. Roncalli, Jérôme Pizzinat, Nathalie Cussac, Daniel Parini, Angelo Mialet-Perez, Jeanne Douin-Echinard, Victorine Selective Cardiomyocyte Oxidative Stress Leads to Bystander Senescence of Cardiac Stromal Cells |
title | Selective Cardiomyocyte Oxidative Stress Leads to Bystander Senescence of Cardiac Stromal Cells |
title_full | Selective Cardiomyocyte Oxidative Stress Leads to Bystander Senescence of Cardiac Stromal Cells |
title_fullStr | Selective Cardiomyocyte Oxidative Stress Leads to Bystander Senescence of Cardiac Stromal Cells |
title_full_unstemmed | Selective Cardiomyocyte Oxidative Stress Leads to Bystander Senescence of Cardiac Stromal Cells |
title_short | Selective Cardiomyocyte Oxidative Stress Leads to Bystander Senescence of Cardiac Stromal Cells |
title_sort | selective cardiomyocyte oxidative stress leads to bystander senescence of cardiac stromal cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7956294/ https://www.ncbi.nlm.nih.gov/pubmed/33668142 http://dx.doi.org/10.3390/ijms22052245 |
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