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Article: Myocardial ischemia/reperfusion injury: Mechanisms of injury and implications for management (Review)

TitleMyocardial ischemia/reperfusion injury: Mechanisms of injury and implications for management (Review)
Authors
KeywordsApoptosis
Autophagy
Ferroptosis
Myocardial ischemia
Reperfusion injury
Issue Date2022
PublisherSpandidos Publications. The Journal's web site is located at http://www.spandidos-publications.com
Citation
Experimental and Therapeutic Medicine, 2022, v. 23 n. 6, p. 430 How to Cite?
AbstractMyocardial infarction is one of the primary causes of mortality in patients with coronary heart disease worldwide. Early treatment of acute myocardial infarction restores blood supply of ischemic myocardium and decreases the mortality risk. However, when the interrupted myocardial blood supply is recovered within a certain period of time, it causes more serious damage to the original ischemic myocardium; this is known as myocardial ischemia/reperfusion injury (MIRI). The pathophysiological mechanisms leading to MIRI are associated with oxidative stress, intracellular calcium overload, energy metabolism disorder, apoptosis, endoplasmic reticulum stress, autophagy, pyroptosis, necroptosis and ferroptosis. These interplay with one another and directly or indirectly lead to aggravation of the effect. In the past, apoptosis and autophagy have attracted more attention but necroptosis and ferroptosis also serve key roles. However, the mechanism of MIRI has not been fully elucidated. The present study reviews the mechanisms underlying MIRI. Based on current understanding of the pathophysiological mechanisms of MIRI, the association between cell death-associated signaling pathways were elaborated, providing direction for investigation of novel targets in clinical treatment.
DescriptionFunding: The present study was supported by The National Natural Science Foundation of China (grant no. 81970247) and the Basic and Applied Basic research of Guangdong Province (grant no. 2019A1515110732)
Persistent Identifierhttp://hdl.handle.net/10722/313270
ISSN
2021 Impact Factor: 2.751
2019 SCImago Journal Rankings: 0.508
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorHe, J-
dc.contributor.authorLiu, D-
dc.contributor.authorZhao, L-
dc.contributor.authorRong, J-
dc.contributor.authorZhang, L-
dc.contributor.authorXia, Z-
dc.date.accessioned2022-06-06T05:48:36Z-
dc.date.available2022-06-06T05:48:36Z-
dc.date.issued2022-
dc.identifier.citationExperimental and Therapeutic Medicine, 2022, v. 23 n. 6, p. 430-
dc.identifier.issn1792-0981-
dc.identifier.urihttp://hdl.handle.net/10722/313270-
dc.descriptionFunding: The present study was supported by The National Natural Science Foundation of China (grant no. 81970247) and the Basic and Applied Basic research of Guangdong Province (grant no. 2019A1515110732)-
dc.description.abstractMyocardial infarction is one of the primary causes of mortality in patients with coronary heart disease worldwide. Early treatment of acute myocardial infarction restores blood supply of ischemic myocardium and decreases the mortality risk. However, when the interrupted myocardial blood supply is recovered within a certain period of time, it causes more serious damage to the original ischemic myocardium; this is known as myocardial ischemia/reperfusion injury (MIRI). The pathophysiological mechanisms leading to MIRI are associated with oxidative stress, intracellular calcium overload, energy metabolism disorder, apoptosis, endoplasmic reticulum stress, autophagy, pyroptosis, necroptosis and ferroptosis. These interplay with one another and directly or indirectly lead to aggravation of the effect. In the past, apoptosis and autophagy have attracted more attention but necroptosis and ferroptosis also serve key roles. However, the mechanism of MIRI has not been fully elucidated. The present study reviews the mechanisms underlying MIRI. Based on current understanding of the pathophysiological mechanisms of MIRI, the association between cell death-associated signaling pathways were elaborated, providing direction for investigation of novel targets in clinical treatment.-
dc.languageeng-
dc.publisherSpandidos Publications. The Journal's web site is located at http://www.spandidos-publications.com-
dc.relation.ispartofExperimental and Therapeutic Medicine-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License-
dc.subjectApoptosis-
dc.subjectAutophagy-
dc.subjectFerroptosis-
dc.subjectMyocardial ischemia-
dc.subjectReperfusion injury-
dc.titleMyocardial ischemia/reperfusion injury: Mechanisms of injury and implications for management (Review)-
dc.typeArticle-
dc.identifier.emailRong, J: jrong@hku.hk-
dc.identifier.emailXia, Z: zyxia@hku.hk-
dc.identifier.authorityRong, J=rp00515-
dc.identifier.authorityXia, Z=rp00532-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3892/etm.2022.11357-
dc.identifier.pmid35607376-
dc.identifier.pmcidPMC9121204-
dc.identifier.hkuros333378-
dc.identifier.volume23-
dc.identifier.issue6-
dc.identifier.spage430-
dc.identifier.epage430-
dc.publisher.placeGreece-

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