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Article: Inhibition of cathepsin S attenuates myocardial ischemia/reperfusion injury by suppressing inflammation and apoptosis

TitleInhibition of cathepsin S attenuates myocardial ischemia/reperfusion injury by suppressing inflammation and apoptosis
Authors
Keywordsapoptosis
cardioprotection
cathepsin S
inflammation
myocardial ischemia
Issue Date2021
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31010
Citation
Journal of Cellular Physiology, 2021, v. 236 n. 2, p. 1309-1320 How to Cite?
AbstractMyocardial ischemia/reperfusion (I/R) injury leads to high mortality and morbidity due to the incomplete understanding of the underlying mechanism and the consequent lack of effective therapy. The present study revealed and validated key candidate genes in relation to inflammation and apoptosis pathways underlying myocardial I/R injury. Cathepsin S was identified as the top hub protein based on the protein-protein interaction analysis, and, thus, its role during myocardial I/R injury was further investigated. Myocardial I/R in mice resulted in significantly increased levels of myocardial injury biomarkers (cardiac troponin I, lactic dehydrogenase, and creatinine kinase-MB) and inflammatory cytokines (interleukin-1 beta [IL-1 beta], IL-6, and tumor necrosis factor-alpha), elevated apoptosis rate, and upregulated protein expression of cleaved caspase-8, cleaved caspase-3, and cleaved poly ADP-ribose polymerase. These abovementioned changes were blocked by two different selective cathepsin S inhibitors, LY3000328 or MIV-247. Moreover, Kaplan-Meier survival plot showed that cathepsin S inhibition improved 21-day survival rate following myocardial I/R injury. This study demonstrated that the inhibition of cathepsin S alleviated myocardial I/R-induced injury by suppressing inflammation and apoptosis, which may be used in clinical applications of cardioprotection.
Persistent Identifierhttp://hdl.handle.net/10722/293665
ISSN
2023 Impact Factor: 4.5
2023 SCImago Journal Rankings: 1.321
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorPeng, K-
dc.contributor.authorLiu, H-
dc.contributor.authorYan, B-
dc.contributor.authorMeng, XW-
dc.contributor.authorSong, SS-
dc.contributor.authorJi, FH-
dc.contributor.authorXia, Z-
dc.date.accessioned2020-11-23T08:20:03Z-
dc.date.available2020-11-23T08:20:03Z-
dc.date.issued2021-
dc.identifier.citationJournal of Cellular Physiology, 2021, v. 236 n. 2, p. 1309-1320-
dc.identifier.issn0021-9541-
dc.identifier.urihttp://hdl.handle.net/10722/293665-
dc.description.abstractMyocardial ischemia/reperfusion (I/R) injury leads to high mortality and morbidity due to the incomplete understanding of the underlying mechanism and the consequent lack of effective therapy. The present study revealed and validated key candidate genes in relation to inflammation and apoptosis pathways underlying myocardial I/R injury. Cathepsin S was identified as the top hub protein based on the protein-protein interaction analysis, and, thus, its role during myocardial I/R injury was further investigated. Myocardial I/R in mice resulted in significantly increased levels of myocardial injury biomarkers (cardiac troponin I, lactic dehydrogenase, and creatinine kinase-MB) and inflammatory cytokines (interleukin-1 beta [IL-1 beta], IL-6, and tumor necrosis factor-alpha), elevated apoptosis rate, and upregulated protein expression of cleaved caspase-8, cleaved caspase-3, and cleaved poly ADP-ribose polymerase. These abovementioned changes were blocked by two different selective cathepsin S inhibitors, LY3000328 or MIV-247. Moreover, Kaplan-Meier survival plot showed that cathepsin S inhibition improved 21-day survival rate following myocardial I/R injury. This study demonstrated that the inhibition of cathepsin S alleviated myocardial I/R-induced injury by suppressing inflammation and apoptosis, which may be used in clinical applications of cardioprotection.-
dc.languageeng-
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31010-
dc.relation.ispartofJournal of Cellular Physiology-
dc.rightsSubmitted (preprint) Version This is the pre-peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article using the DOI]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. Accepted (peer-reviewed) Version This is the peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article using the DOI]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.-
dc.subjectapoptosis-
dc.subjectcardioprotection-
dc.subjectcathepsin S-
dc.subjectinflammation-
dc.subjectmyocardial ischemia-
dc.titleInhibition of cathepsin S attenuates myocardial ischemia/reperfusion injury by suppressing inflammation and apoptosis-
dc.typeArticle-
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hk-
dc.identifier.authorityXia, Z=rp00532-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/jcp.29938-
dc.identifier.pmid32657442-
dc.identifier.scopuseid_2-s2.0-85087748439-
dc.identifier.hkuros319753-
dc.identifier.volume236-
dc.identifier.issue2-
dc.identifier.spage1309-
dc.identifier.epage1320-
dc.identifier.isiWOS:000591221500043-
dc.publisher.placeUnited States-

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