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PGC‐1α protects from myocardial ischaemia‐reperfusion injury by regulating mitonuclear communication
The recovery of blood supply after a period of myocardial ischaemia does not restore the heart function and instead results in a serious dysfunction called myocardial ischaemia‐reperfusion injury (IRI), which involves several complex pathophysiological processes. Mitochondria have a wide range of fu...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8817131/ https://www.ncbi.nlm.nih.gov/pubmed/33470050 http://dx.doi.org/10.1111/jcmm.16236 |
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author | Li, Yan‐Qing Jiao, Yan Liu, Ya‐Nan Fu, Jia‐ying Sun, Lian‐Kun Su, Jing |
author_facet | Li, Yan‐Qing Jiao, Yan Liu, Ya‐Nan Fu, Jia‐ying Sun, Lian‐Kun Su, Jing |
author_sort | Li, Yan‐Qing |
collection | PubMed |
description | The recovery of blood supply after a period of myocardial ischaemia does not restore the heart function and instead results in a serious dysfunction called myocardial ischaemia‐reperfusion injury (IRI), which involves several complex pathophysiological processes. Mitochondria have a wide range of functions in maintaining the cellular energy supply, cell signalling and programmed cell death. When mitochondrial function is insufficient or disordered, it may have adverse effects on myocardial ischaemia‐reperfusion and therefore mitochondrial dysfunction caused by oxidative stress a core molecular mechanism of IRI. Peroxisome proliferator‐activated receptor gamma co‐activator 1α (PGC‐1α) is an important antioxidant molecule found in mitochondria. However, its role in IRI has not yet been systematically summarized. In this review, we speculate the role of PGC‐1α as a key regulator of mitonuclear communication, which may interacts with nuclear factor, erythroid 2 like ‐1 and ‐2 (NRF‐1/2) to inhibit mitochondrial oxidative stress, promote the clearance of damaged mitochondria, enhance mitochondrial biogenesis, and reduce the burden of IRI. |
format | Online Article Text |
id | pubmed-8817131 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-88171312022-02-08 PGC‐1α protects from myocardial ischaemia‐reperfusion injury by regulating mitonuclear communication Li, Yan‐Qing Jiao, Yan Liu, Ya‐Nan Fu, Jia‐ying Sun, Lian‐Kun Su, Jing J Cell Mol Med Reviews The recovery of blood supply after a period of myocardial ischaemia does not restore the heart function and instead results in a serious dysfunction called myocardial ischaemia‐reperfusion injury (IRI), which involves several complex pathophysiological processes. Mitochondria have a wide range of functions in maintaining the cellular energy supply, cell signalling and programmed cell death. When mitochondrial function is insufficient or disordered, it may have adverse effects on myocardial ischaemia‐reperfusion and therefore mitochondrial dysfunction caused by oxidative stress a core molecular mechanism of IRI. Peroxisome proliferator‐activated receptor gamma co‐activator 1α (PGC‐1α) is an important antioxidant molecule found in mitochondria. However, its role in IRI has not yet been systematically summarized. In this review, we speculate the role of PGC‐1α as a key regulator of mitonuclear communication, which may interacts with nuclear factor, erythroid 2 like ‐1 and ‐2 (NRF‐1/2) to inhibit mitochondrial oxidative stress, promote the clearance of damaged mitochondria, enhance mitochondrial biogenesis, and reduce the burden of IRI. John Wiley and Sons Inc. 2021-01-19 2022-02 /pmc/articles/PMC8817131/ /pubmed/33470050 http://dx.doi.org/10.1111/jcmm.16236 Text en © 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Reviews Li, Yan‐Qing Jiao, Yan Liu, Ya‐Nan Fu, Jia‐ying Sun, Lian‐Kun Su, Jing PGC‐1α protects from myocardial ischaemia‐reperfusion injury by regulating mitonuclear communication |
title | PGC‐1α protects from myocardial ischaemia‐reperfusion injury by regulating mitonuclear communication |
title_full | PGC‐1α protects from myocardial ischaemia‐reperfusion injury by regulating mitonuclear communication |
title_fullStr | PGC‐1α protects from myocardial ischaemia‐reperfusion injury by regulating mitonuclear communication |
title_full_unstemmed | PGC‐1α protects from myocardial ischaemia‐reperfusion injury by regulating mitonuclear communication |
title_short | PGC‐1α protects from myocardial ischaemia‐reperfusion injury by regulating mitonuclear communication |
title_sort | pgc‐1α protects from myocardial ischaemia‐reperfusion injury by regulating mitonuclear communication |
topic | Reviews |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8817131/ https://www.ncbi.nlm.nih.gov/pubmed/33470050 http://dx.doi.org/10.1111/jcmm.16236 |
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