Musclin attenuates lipid deposition in hepatocytes through SIRT7/autophagy-mediated suppression of ER stress
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Cho, Wonjun | - |
dc.contributor.author | Choi, Sung Woo | - |
dc.contributor.author | Oh, Heeseung | - |
dc.contributor.author | Baygutalp, Fatih | - |
dc.contributor.author | Abd El-Aty, A.M. | - |
dc.contributor.author | Jeong, Ji Hoon | - |
dc.contributor.author | Song, Jin-Ho | - |
dc.contributor.author | Shin, Yong Kyoo | - |
dc.contributor.author | Jung, Tae Woo | - |
dc.date.accessioned | 2024-01-09T04:10:30Z | - |
dc.date.available | 2024-01-09T04:10:30Z | - |
dc.date.issued | 2023-05 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.issn | 1090-2104 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/69869 | - |
dc.description.abstract | Musclin, an exercise-responsive myokine, has the ability to attenuate inflammation, oxidative stress, and apoptosis in cardiomyocytes under pathogenic conditions. While the potential benefits of musclin in the cardiovascular system have been well documented, its effects on hepatic endoplasmic reticulum (ER) stress and lipid metabolism are not fully understood. The present study showed that musclin treatment reduced lipid accumulation and lipogenic protein expression in primary hepatocytes exposed to palmitate. Palmitate treatment led to an increase in markers of ER stress, which was reversed by musclin treatment. Musclin treatment increased SIRT7 expression and markers of autophagy in a dose-dependent manner. Small interfering (si) RNA of SIRT7 or 3-methyladenine (3 MA) reduced the effects of musclin on lipogenic lipid deposition in hepatocytes under hyperlipidemic conditions. These findings suggest that musclin can suppress palmitate-induced ER stress by upregulating SIRT7 and autophagy signaling, thereby alleviating lipid accumulation in primary hepatocytes. The current study provides a potential therapeutic strategy for the treatment of liver diseases characterized by lipid accumulation and ER stress, such as nonalcoholic fatty liver disease (NAFLD). © 2023 Elsevier Inc. | - |
dc.format.extent | 7 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | Elsevier B.V. | - |
dc.title | Musclin attenuates lipid deposition in hepatocytes through SIRT7/autophagy-mediated suppression of ER stress | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.bbrc.2023.03.065 | - |
dc.identifier.bibliographicCitation | Biochemical and Biophysical Research Communications, v.658, pp 62 - 68 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000976618600001 | - |
dc.identifier.scopusid | 2-s2.0-85151535543 | - |
dc.citation.endPage | 68 | - |
dc.citation.startPage | 62 | - |
dc.citation.title | Biochemical and Biophysical Research Communications | - |
dc.citation.volume | 658 | - |
dc.type.docType | Article | - |
dc.publisher.location | 미국 | - |
dc.subject.keywordAuthor | Hepatocyte | - |
dc.subject.keywordAuthor | Lipogenesis | - |
dc.subject.keywordAuthor | Musclin | - |
dc.subject.keywordAuthor | NAFLD | - |
dc.subject.keywordAuthor | Obesity | - |
dc.subject.keywordPlus | OSTEOCRIN | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | PROTECTS | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Biophysics | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biophysics | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
84, Heukseok-ro, Dongjak-gu, Seoul, Republic of Korea (06974)02-820-6194
COPYRIGHT 2019 Chung-Ang 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.