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Non-coding RNAs modulate autophagy in myocardial ischemia-reperfusion injury: a systematic review

The myocardial infarction is the main cause of morbidity and mortality in cardiovascular diseases around the world. Although the timely and complete reperfusion via Percutaneous Coronary Intervention (PCI) or thrombolysis have distinctly decreased the mortality of myocardial infarction, reperfusion...

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Autores principales: Huang, Fuwen, Mai, Jingting, Chen, Jingwei, He, Yinying, Chen, Xiaojun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8141194/
https://www.ncbi.nlm.nih.gov/pubmed/34022925
http://dx.doi.org/10.1186/s13019-021-01524-9
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author Huang, Fuwen
Mai, Jingting
Chen, Jingwei
He, Yinying
Chen, Xiaojun
author_facet Huang, Fuwen
Mai, Jingting
Chen, Jingwei
He, Yinying
Chen, Xiaojun
author_sort Huang, Fuwen
collection PubMed
description The myocardial infarction is the main cause of morbidity and mortality in cardiovascular diseases around the world. Although the timely and complete reperfusion via Percutaneous Coronary Intervention (PCI) or thrombolysis have distinctly decreased the mortality of myocardial infarction, reperfusion itself may lead to supererogatory irreversible myocardial injury and heart function disorders, namely ischemia-reperfusion (I/R) injury. Extensive studies have indicated that non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs), play important roles in the progress of myocardial I/R injury, which is closely correlative with cardiomyocytes autophagy. Moreover, autophagy plays an important role in maintaining homeostasis and protecting cells in the myocardial ischemia reperfusion and cardiomyocyte hypoxia-reoxygenation (H/R) progress. In this review, we first introduced the biogenesis and functions of ncRNAs, and subsequently summarized the roles and relevant molecular mechanisms of ncRNAs regulating autophagy in myocardial I/R injury. We hope that this review in addition to develop a better understanding of the physiological and pathological roles of ncRNAs, can also lay a foundation for the therapies of myocardial I/R injury, and even for other related cardiovascular diseases.
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spelling pubmed-81411942021-05-25 Non-coding RNAs modulate autophagy in myocardial ischemia-reperfusion injury: a systematic review Huang, Fuwen Mai, Jingting Chen, Jingwei He, Yinying Chen, Xiaojun J Cardiothorac Surg Review The myocardial infarction is the main cause of morbidity and mortality in cardiovascular diseases around the world. Although the timely and complete reperfusion via Percutaneous Coronary Intervention (PCI) or thrombolysis have distinctly decreased the mortality of myocardial infarction, reperfusion itself may lead to supererogatory irreversible myocardial injury and heart function disorders, namely ischemia-reperfusion (I/R) injury. Extensive studies have indicated that non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs), play important roles in the progress of myocardial I/R injury, which is closely correlative with cardiomyocytes autophagy. Moreover, autophagy plays an important role in maintaining homeostasis and protecting cells in the myocardial ischemia reperfusion and cardiomyocyte hypoxia-reoxygenation (H/R) progress. In this review, we first introduced the biogenesis and functions of ncRNAs, and subsequently summarized the roles and relevant molecular mechanisms of ncRNAs regulating autophagy in myocardial I/R injury. We hope that this review in addition to develop a better understanding of the physiological and pathological roles of ncRNAs, can also lay a foundation for the therapies of myocardial I/R injury, and even for other related cardiovascular diseases. BioMed Central 2021-05-22 /pmc/articles/PMC8141194/ /pubmed/34022925 http://dx.doi.org/10.1186/s13019-021-01524-9 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Review
Huang, Fuwen
Mai, Jingting
Chen, Jingwei
He, Yinying
Chen, Xiaojun
Non-coding RNAs modulate autophagy in myocardial ischemia-reperfusion injury: a systematic review
title Non-coding RNAs modulate autophagy in myocardial ischemia-reperfusion injury: a systematic review
title_full Non-coding RNAs modulate autophagy in myocardial ischemia-reperfusion injury: a systematic review
title_fullStr Non-coding RNAs modulate autophagy in myocardial ischemia-reperfusion injury: a systematic review
title_full_unstemmed Non-coding RNAs modulate autophagy in myocardial ischemia-reperfusion injury: a systematic review
title_short Non-coding RNAs modulate autophagy in myocardial ischemia-reperfusion injury: a systematic review
title_sort non-coding rnas modulate autophagy in myocardial ischemia-reperfusion injury: a systematic review
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8141194/
https://www.ncbi.nlm.nih.gov/pubmed/34022925
http://dx.doi.org/10.1186/s13019-021-01524-9
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