Effects of a proteasome inhibitor on cardiomyocytes in a pressure-overload hypertrophy rat model: An animal study
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, I.-S. | - |
dc.contributor.author | Jo, W.-M. | - |
dc.date.accessioned | 2021-09-03T14:05:50Z | - |
dc.date.available | 2021-09-03T14:05:50Z | - |
dc.date.created | 2021-06-17 | - |
dc.date.issued | 2017 | - |
dc.identifier.issn | 2233-601X | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/86114 | - |
dc.description.abstract | Background: The ubiquitin-proteasome system (UPS) is an important pathway of proteolysis in pathologic hypertrophic cardiomyocytes. We hypothesize that MG132, a proteasome inhibitor, might prevent hypertrophic cardiomyopathy (CMP) by blocking the UPS. Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and androgen receptor (AR) have been reported to be mediators of CMP and heart failure. This study drew upon pathophysiologic studies and the analysis of NF-κB and AR to assess the cardioprotective effects of MG132 in a left ventricular hypertrophy (LVH) rat model. Methods: We constructed a transverse aortic constriction (TAC)-induced LVH rat model with 3 groups: sham (TAC-sham, n=10), control (TAC-cont, n=10), and MG132 administration (TAC-MG132, n=10). MG-132 (0.1 mg/kg) was injected for 4 weeks in the TAC-MG132 group. Pathophysiologic evaluations were performed and the expression of AR and NF-κB was measured in the left ventricle. Results: Fibrosis was prevalent in the pathologic examination of the TAC-cont model, and it was reduced in the TAC-MG132 group, although not significantly. Less expression of AR, but not NF-κB, was found in the TAC-MG132 group than in the TAC-cont group (p<0.05). Conclusion: MG-132 was found to suppress AR in the TAC-CMP model by blocking the UPS, which reduced fibrosis. However, NF-κB expression levels were not related to UPS function. © The Korean Society for Thoracic and Cardiovascular Surgery. 2017. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | Korean Society for Thoracic and Cardiovascular Surgery | - |
dc.title | Effects of a proteasome inhibitor on cardiomyocytes in a pressure-overload hypertrophy rat model: An animal study | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Jo, W.-M. | - |
dc.identifier.doi | 10.5090/kjtcs.2017.50.3.144 | - |
dc.identifier.scopusid | 2-s2.0-85020057053 | - |
dc.identifier.bibliographicCitation | Korean Journal of Thoracic and Cardiovascular Surgery, v.50, no.3, pp.144 - 152 | - |
dc.relation.isPartOf | Korean Journal of Thoracic and Cardiovascular Surgery | - |
dc.citation.title | Korean Journal of Thoracic and Cardiovascular Surgery | - |
dc.citation.volume | 50 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 144 | - |
dc.citation.endPage | 152 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.identifier.kciid | ART002229435 | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scopus | - |
dc.description.journalRegisteredClass | kci | - |
dc.subject.keywordAuthor | Androgen | - |
dc.subject.keywordAuthor | Cardiomyopathy | - |
dc.subject.keywordAuthor | Hypertrophic | - |
dc.subject.keywordAuthor | MG132 | - |
dc.subject.keywordAuthor | NF-kappa B | - |
dc.subject.keywordAuthor | Proteasome inhibitors | - |
dc.subject.keywordAuthor | Receptors | - |
dc.subject.keywordAuthor | Ubiquitins | - |
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