Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury
Mitochondria are the central target of ischemic preconditioning and postconditioning cardioprotective strategies, which consist of either the application of brief intermittent ischemia/reperfusion (I/R) cycles or the administration of pharmacological agents. Such strategies reduce cardiac I/R injury...
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MDPI AG
2021-10-01
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Series: | Life |
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Online Access: | https://www.mdpi.com/2075-1729/11/11/1123 |
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author | Wylly Ramsés García-Niño Cecilia Zazueta Mabel Buelna-Chontal Alejandro Silva-Palacios |
author_facet | Wylly Ramsés García-Niño Cecilia Zazueta Mabel Buelna-Chontal Alejandro Silva-Palacios |
author_sort | Wylly Ramsés García-Niño |
collection | DOAJ |
description | Mitochondria are the central target of ischemic preconditioning and postconditioning cardioprotective strategies, which consist of either the application of brief intermittent ischemia/reperfusion (I/R) cycles or the administration of pharmacological agents. Such strategies reduce cardiac I/R injury by activating protective signaling pathways that prevent the exacerbated production of reactive oxygen/nitrogen species, inhibit opening of mitochondrial permeability transition pore and reduce apoptosis, maintaining normal mitochondrial function. Cardioprotection also involves the activation of mitochondrial quality control (MQC) processes, which replace defective mitochondria or eliminate mitochondrial debris, preserving the structure and function of the network of these organelles, and consequently ensuring homeostasis and survival of cardiomyocytes. Such processes include mitochondrial biogenesis, fission, fusion, mitophagy and mitochondrial-controlled cell death. This review updates recent advances in MQC mechanisms that are activated in the protection conferred by different cardiac conditioning interventions. Furthermore, the role of extracellular vesicles in mitochondrial protection and turnover of these organelles will be discussed. It is concluded that modulation of MQC mechanisms and recognition of mitochondrial targets could provide a potential and selective therapeutic approach for I/R-induced mitochondrial dysfunction. |
first_indexed | 2024-03-10T05:21:08Z |
format | Article |
id | doaj.art-dbb21420bd6d4696aa2fe7b1a70bb9fe |
institution | Directory Open Access Journal |
issn | 2075-1729 |
language | English |
last_indexed | 2024-03-10T05:21:08Z |
publishDate | 2021-10-01 |
publisher | MDPI AG |
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series | Life |
spelling | doaj.art-dbb21420bd6d4696aa2fe7b1a70bb9fe2023-11-23T00:03:07ZengMDPI AGLife2075-17292021-10-011111112310.3390/life11111123Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion InjuryWylly Ramsés García-Niño0Cecilia Zazueta1Mabel Buelna-Chontal2Alejandro Silva-Palacios3Department of Cardiovascular Biomedicine, National Institute of Cardiology “Ignacio Chávez”, Mexico City 14080, MexicoDepartment of Cardiovascular Biomedicine, National Institute of Cardiology “Ignacio Chávez”, Mexico City 14080, MexicoDepartment of Cardiovascular Biomedicine, National Institute of Cardiology “Ignacio Chávez”, Mexico City 14080, MexicoDepartment of Cardiovascular Biomedicine, National Institute of Cardiology “Ignacio Chávez”, Mexico City 14080, MexicoMitochondria are the central target of ischemic preconditioning and postconditioning cardioprotective strategies, which consist of either the application of brief intermittent ischemia/reperfusion (I/R) cycles or the administration of pharmacological agents. Such strategies reduce cardiac I/R injury by activating protective signaling pathways that prevent the exacerbated production of reactive oxygen/nitrogen species, inhibit opening of mitochondrial permeability transition pore and reduce apoptosis, maintaining normal mitochondrial function. Cardioprotection also involves the activation of mitochondrial quality control (MQC) processes, which replace defective mitochondria or eliminate mitochondrial debris, preserving the structure and function of the network of these organelles, and consequently ensuring homeostasis and survival of cardiomyocytes. Such processes include mitochondrial biogenesis, fission, fusion, mitophagy and mitochondrial-controlled cell death. This review updates recent advances in MQC mechanisms that are activated in the protection conferred by different cardiac conditioning interventions. Furthermore, the role of extracellular vesicles in mitochondrial protection and turnover of these organelles will be discussed. It is concluded that modulation of MQC mechanisms and recognition of mitochondrial targets could provide a potential and selective therapeutic approach for I/R-induced mitochondrial dysfunction.https://www.mdpi.com/2075-1729/11/11/1123myocardial infarctionischemic preconditioningischemic postconditioningcardioprotectionmitochondrial biogenesismitochondrial dynamics |
spellingShingle | Wylly Ramsés García-Niño Cecilia Zazueta Mabel Buelna-Chontal Alejandro Silva-Palacios Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury Life myocardial infarction ischemic preconditioning ischemic postconditioning cardioprotection mitochondrial biogenesis mitochondrial dynamics |
title | Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury |
title_full | Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury |
title_fullStr | Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury |
title_full_unstemmed | Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury |
title_short | Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury |
title_sort | mitochondrial quality control in cardiac conditioning strategies against ischemia reperfusion injury |
topic | myocardial infarction ischemic preconditioning ischemic postconditioning cardioprotection mitochondrial biogenesis mitochondrial dynamics |
url | https://www.mdpi.com/2075-1729/11/11/1123 |
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