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Noncoding RNAs in Cardiac Autophagy following Myocardial Infarction

Macroautophagy is an evolutionarily conserved process of the lysosome-dependent degradation of damaged proteins and organelles and plays an important role in cellular homeostasis. Macroautophagy is upregulated after myocardial infarction (MI) and seems to be detrimental during reperfusion and protec...

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Autores principales: Turkieh, Annie, Charrier, Henri, Dubois-Deruy, Emilie, Porouchani, Sina, Bouvet, Marion, Pinet, Florence
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6589265/
https://www.ncbi.nlm.nih.gov/pubmed/31341537
http://dx.doi.org/10.1155/2019/8438650
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author Turkieh, Annie
Charrier, Henri
Dubois-Deruy, Emilie
Porouchani, Sina
Bouvet, Marion
Pinet, Florence
author_facet Turkieh, Annie
Charrier, Henri
Dubois-Deruy, Emilie
Porouchani, Sina
Bouvet, Marion
Pinet, Florence
author_sort Turkieh, Annie
collection PubMed
description Macroautophagy is an evolutionarily conserved process of the lysosome-dependent degradation of damaged proteins and organelles and plays an important role in cellular homeostasis. Macroautophagy is upregulated after myocardial infarction (MI) and seems to be detrimental during reperfusion and protective during left ventricle remodeling. Identifying new regulators of cardiac autophagy may help to maintain the activity of this process and protect the heart from MI effects. Recently, it was shown that noncoding RNAs (microRNAs and long noncoding RNAs) are involved in autophagy regulation in different cell types including cardiac cells. In this review, we summarized the role of macroautophagy in the heart following MI and we focused on the noncoding RNAs and their targeted genes reported to regulate autophagy in the heart under these pathological conditions.
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spelling pubmed-65892652019-07-24 Noncoding RNAs in Cardiac Autophagy following Myocardial Infarction Turkieh, Annie Charrier, Henri Dubois-Deruy, Emilie Porouchani, Sina Bouvet, Marion Pinet, Florence Oxid Med Cell Longev Review Article Macroautophagy is an evolutionarily conserved process of the lysosome-dependent degradation of damaged proteins and organelles and plays an important role in cellular homeostasis. Macroautophagy is upregulated after myocardial infarction (MI) and seems to be detrimental during reperfusion and protective during left ventricle remodeling. Identifying new regulators of cardiac autophagy may help to maintain the activity of this process and protect the heart from MI effects. Recently, it was shown that noncoding RNAs (microRNAs and long noncoding RNAs) are involved in autophagy regulation in different cell types including cardiac cells. In this review, we summarized the role of macroautophagy in the heart following MI and we focused on the noncoding RNAs and their targeted genes reported to regulate autophagy in the heart under these pathological conditions. Hindawi 2019-06-03 /pmc/articles/PMC6589265/ /pubmed/31341537 http://dx.doi.org/10.1155/2019/8438650 Text en Copyright © 2019 Annie Turkieh et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Turkieh, Annie
Charrier, Henri
Dubois-Deruy, Emilie
Porouchani, Sina
Bouvet, Marion
Pinet, Florence
Noncoding RNAs in Cardiac Autophagy following Myocardial Infarction
title Noncoding RNAs in Cardiac Autophagy following Myocardial Infarction
title_full Noncoding RNAs in Cardiac Autophagy following Myocardial Infarction
title_fullStr Noncoding RNAs in Cardiac Autophagy following Myocardial Infarction
title_full_unstemmed Noncoding RNAs in Cardiac Autophagy following Myocardial Infarction
title_short Noncoding RNAs in Cardiac Autophagy following Myocardial Infarction
title_sort noncoding rnas in cardiac autophagy following myocardial infarction
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6589265/
https://www.ncbi.nlm.nih.gov/pubmed/31341537
http://dx.doi.org/10.1155/2019/8438650
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