Inhibition of miR-25 Ameliorates Cardiac Dysfunction and Fibrosis by Restoring Kruppel-like Factor 4 Expression
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, Cholong | - |
dc.contributor.author | Cho, Sunghye | - |
dc.contributor.author | Jeong, Dongtak | - |
dc.date.accessioned | 2023-09-18T05:31:45Z | - |
dc.date.available | 2023-09-18T05:31:45Z | - |
dc.date.issued | 2023-08 | - |
dc.identifier.issn | 1661-6596 | - |
dc.identifier.issn | 1422-0067 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/115330 | - |
dc.description.abstract | Cardiac hypertrophy is an adaptive response to various pathological insults, including hypertension. However, sustained hypertrophy can cause impaired calcium regulation, cardiac dysfunction, and remodeling, accompanied by cardiac fibrosis. Our previous study identified miR-25 as a regulator of SERCA2a, and found that the inhibition of miR-25 improved cardiac function and reduced fibrosis by restoring SERCA2a expression in a murine heart failure model. However, the precise mechanism underlying the reduction in fibrosis following miR-25 inhibition remains unclear. Therefore, we postulate that miR-25 may have additional targets that contribute to regulating cardiac fibrosis. Using in silico analysis, Kruppel-like factor 4 (KLF4) was identified as an additional target of miR-25. Further experiments confirmed that KLF4 was directly targeted by miR-25 and that its expression was reduced by long-term treatment with Angiotensin II, a major hypertrophic inducer. Subsequently, treatment with an miR-25 inhibitor alleviated the cardiac dysfunction, fibrosis, and inflammation induced by Angiotensin II (Ang II). These findings indicate that inhibiting miR-25 not only enhances calcium cycling and cardiac function via SERCA2a restoration but also reduces fibrosis by restoring KLF4 expression. Therefore, targeting miR-25 may be a promising therapeutic strategy for treating hypertensive heart diseases. | - |
dc.format.extent | 15 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | Multidisciplinary Digital Publishing Institute (MDPI) | - |
dc.title | Inhibition of miR-25 Ameliorates Cardiac Dysfunction and Fibrosis by Restoring Kruppel-like Factor 4 Expression | - |
dc.type | Article | - |
dc.publisher.location | 스위스 | - |
dc.identifier.doi | 10.3390/ijms241512434 | - |
dc.identifier.scopusid | 2-s2.0-85167745028 | - |
dc.identifier.wosid | 001045563300001 | - |
dc.identifier.bibliographicCitation | International Journal of Molecular Sciences, v.24, no.15, pp 1 - 15 | - |
dc.citation.title | International Journal of Molecular Sciences | - |
dc.citation.volume | 24 | - |
dc.citation.number | 15 | - |
dc.citation.startPage | 1 | - |
dc.citation.endPage | 15 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | Y | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Chemistry | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Multidisciplinary | - |
dc.subject.keywordPlus | INDUCED CARDIOMYOCYTE HYPERTROPHY | - |
dc.subject.keywordPlus | HEART | - |
dc.subject.keywordPlus | KLF4 | - |
dc.subject.keywordPlus | KRUPPEL-LIKE-FACTOR-4 | - |
dc.subject.keywordPlus | HYPERTENSION | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | MACROPHAGES | - |
dc.subject.keywordPlus | PROGRESSION | - |
dc.subject.keywordPlus | PRESSURE | - |
dc.subject.keywordAuthor | cardiac dysfunction | - |
dc.subject.keywordAuthor | hypertension | - |
dc.subject.keywordAuthor | cardiac hypertrophy | - |
dc.subject.keywordAuthor | cardiac fibrosis | - |
dc.subject.keywordAuthor | miR-25 | - |
dc.subject.keywordAuthor | KLF4 | - |
dc.subject.keywordAuthor | Angiotensin II | - |
dc.subject.keywordAuthor | inflammation | - |
dc.subject.keywordAuthor | SERCA2a | - |
dc.identifier.url | https://www.mdpi.com/1422-0067/24/15/12434 | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
55 Hanyangdeahak-ro, Sangnok-gu, Ansan, Gyeonggi-do, 15588, Korea+82-31-400-4269 sweetbrain@hanyang.ac.kr
COPYRIGHT © 2021 HANYANG UNIVERSITY. ALL RIGHTS RESERVED.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.