Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic Preconditioning
It is now well established that ischemia/reperfusion (I/R) injury is associated with the compromised recovery of cardiac contractile function. Such an adverse effect of I/R injury in the heart is attributed to the development of oxidative stress and intracellular Ca<sup>2+</sup>-overload...
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MDPI AG
2022-03-01
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author | Paramjit S. Tappia Anureet K. Shah Bram Ramjiawan Naranjan S. Dhalla |
author_facet | Paramjit S. Tappia Anureet K. Shah Bram Ramjiawan Naranjan S. Dhalla |
author_sort | Paramjit S. Tappia |
collection | DOAJ |
description | It is now well established that ischemia/reperfusion (I/R) injury is associated with the compromised recovery of cardiac contractile function. Such an adverse effect of I/R injury in the heart is attributed to the development of oxidative stress and intracellular Ca<sup>2+</sup>-overload, which are known to induce remodeling of subcellular organelles such as sarcolemma, sarcoplasmic reticulum, mitochondria and myofibrils. However, repeated episodes of brief periods of ischemia followed by reperfusion or ischemic preconditioning (IP) have been shown to improve cardiac function and exert cardioprotective actions against the adverse effects of prolonged I/R injury. This protective action of IP in attenuating myocardial damage and subcellular remodeling is likely to be due to marked reductions in the occurrence of oxidative stress and intracellular Ca<sup>2+</sup>-overload in cardiomyocytes. In addition, the beneficial actions of IP have been attributed to the depression of proteolytic activities and inflammatory levels of cytokines as well as the activation of the nuclear factor erythroid factor 2-mediated signal transduction pathway. Accordingly, this review is intended to describe some of the changes in subcellular organelles, which are induced in cardiomyocytes by I/R for the occurrence of oxidative stress and intracellular Ca<sup>2+</sup>-overload and highlight some of the mechanisms for explaining the cardioprotective effects of IP. |
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issn | 1661-6596 1422-0067 |
language | English |
last_indexed | 2024-03-09T11:49:05Z |
publishDate | 2022-03-01 |
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series | International Journal of Molecular Sciences |
spelling | doaj.art-097af8ef804a40b3b981bd8c04fb44432023-11-30T23:16:43ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-03-01237342510.3390/ijms23073425Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic PreconditioningParamjit S. Tappia0Anureet K. Shah1Bram Ramjiawan2Naranjan S. Dhalla3Asper Clinical Research Institute, St. Boniface Hospital, Winnipeg, MB R2H 2A6, CanadaDepartment of Kinesiology, Nutrition and Food Science, California State University, Los Angeles, CA 90032, USAAsper Clinical Research Institute, St. Boniface Hospital, Winnipeg, MB R2H 2A6, CanadaSt. Boniface Hospital Albrechtsen Research Centre, Department of Physiology and Pathophysiology, Institute of Cardiovascular Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB R2H 2A6, CanadaIt is now well established that ischemia/reperfusion (I/R) injury is associated with the compromised recovery of cardiac contractile function. Such an adverse effect of I/R injury in the heart is attributed to the development of oxidative stress and intracellular Ca<sup>2+</sup>-overload, which are known to induce remodeling of subcellular organelles such as sarcolemma, sarcoplasmic reticulum, mitochondria and myofibrils. However, repeated episodes of brief periods of ischemia followed by reperfusion or ischemic preconditioning (IP) have been shown to improve cardiac function and exert cardioprotective actions against the adverse effects of prolonged I/R injury. This protective action of IP in attenuating myocardial damage and subcellular remodeling is likely to be due to marked reductions in the occurrence of oxidative stress and intracellular Ca<sup>2+</sup>-overload in cardiomyocytes. In addition, the beneficial actions of IP have been attributed to the depression of proteolytic activities and inflammatory levels of cytokines as well as the activation of the nuclear factor erythroid factor 2-mediated signal transduction pathway. Accordingly, this review is intended to describe some of the changes in subcellular organelles, which are induced in cardiomyocytes by I/R for the occurrence of oxidative stress and intracellular Ca<sup>2+</sup>-overload and highlight some of the mechanisms for explaining the cardioprotective effects of IP.https://www.mdpi.com/1422-0067/23/7/3425ischemia-reperfusion injurysubcellular remodelingischemic preconditioningcardioprotectionoxidative stressintracellular Ca<sup>2+</sup>-overload |
spellingShingle | Paramjit S. Tappia Anureet K. Shah Bram Ramjiawan Naranjan S. Dhalla Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic Preconditioning International Journal of Molecular Sciences ischemia-reperfusion injury subcellular remodeling ischemic preconditioning cardioprotection oxidative stress intracellular Ca<sup>2+</sup>-overload |
title | Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic Preconditioning |
title_full | Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic Preconditioning |
title_fullStr | Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic Preconditioning |
title_full_unstemmed | Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic Preconditioning |
title_short | Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic Preconditioning |
title_sort | modification of ischemia reperfusion induced alterations in subcellular organelles by ischemic preconditioning |
topic | ischemia-reperfusion injury subcellular remodeling ischemic preconditioning cardioprotection oxidative stress intracellular Ca<sup>2+</sup>-overload |
url | https://www.mdpi.com/1422-0067/23/7/3425 |
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