靶向衰竭心脏中代谢激活的成纤维细胞

IF 9.4 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Nature cardiovascular research Pub Date : 2024-07-05 DOI:10.1038/s44161-024-00500-5
Nikolaos G. Frangogiannis
{"title":"靶向衰竭心脏中代谢激活的成纤维细胞","authors":"Nikolaos G. Frangogiannis","doi":"10.1038/s44161-024-00500-5","DOIUrl":null,"url":null,"abstract":"Myofibroblast activation requires nuclear translocation of ATP citrate lyase (ACLY) that triggers chromatin remodeling and the induction of fibrosis-associated genes. ACLY inhibition prevents myofibroblast conversion and causes de-differentiation of myofibroblasts to fibroblasts, indicating a potential therapeutic approach for heart failure.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 7","pages":"782-784"},"PeriodicalIF":9.4000,"publicationDate":"2024-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Targeting metabolically activated fibroblasts in the failing heart\",\"authors\":\"Nikolaos G. Frangogiannis\",\"doi\":\"10.1038/s44161-024-00500-5\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Myofibroblast activation requires nuclear translocation of ATP citrate lyase (ACLY) that triggers chromatin remodeling and the induction of fibrosis-associated genes. ACLY inhibition prevents myofibroblast conversion and causes de-differentiation of myofibroblasts to fibroblasts, indicating a potential therapeutic approach for heart failure.\",\"PeriodicalId\":74245,\"journal\":{\"name\":\"Nature cardiovascular research\",\"volume\":\"3 7\",\"pages\":\"782-784\"},\"PeriodicalIF\":9.4000,\"publicationDate\":\"2024-07-05\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nature cardiovascular research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.nature.com/articles/s44161-024-00500-5\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CARDIAC & CARDIOVASCULAR SYSTEMS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nature cardiovascular research","FirstCategoryId":"1085","ListUrlMain":"https://www.nature.com/articles/s44161-024-00500-5","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0

摘要

肌成纤维细胞的活化需要柠檬酸ATP裂解酶(ACLY)的核转位,从而引发染色质重塑和纤维化相关基因的诱导。抑制ACLY可防止肌成纤维细胞转化,并使肌成纤维细胞向成纤维细胞去分化,这表明这是治疗心力衰竭的一种潜在方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

摘要图片

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Targeting metabolically activated fibroblasts in the failing heart
Myofibroblast activation requires nuclear translocation of ATP citrate lyase (ACLY) that triggers chromatin remodeling and the induction of fibrosis-associated genes. ACLY inhibition prevents myofibroblast conversion and causes de-differentiation of myofibroblasts to fibroblasts, indicating a potential therapeutic approach for heart failure.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
CiteScore
5.70
自引率
0.00%
发文量
0
期刊最新文献
Integrative proteomic analyses across common cardiac diseases yield mechanistic insights and enhanced prediction. Genetic and phenotypic architecture of human myocardial trabeculation. Intrinsic GATA4 expression sensitizes the aortic root to dilation in a Loeys-Dietz syndrome mouse model. GLS2 links glutamine metabolism and atherosclerosis by remodeling artery walls. Glutamine-glutamate imbalance in the pathogenesis of cardiovascular disease.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1