科研成果详情

题名ATF3 affects myocardial fibrosis remodeling after myocardial infarction by regulating autophagy and its mechanism of action
作者
发表日期2023-11-15
发表期刊Gene   影响因子和分区
语种英语
原始文献类型Journal Article
关键词ATF3 Autophagy Cardiac remodeling Myocardial fibrosis Myocardial infarction
其他关键词CARDIAC FIBROSIS ; HEART-FAILURE ; REPAIR ; FIBROBLASTS ; PROTECTS
摘要Myocardial fibrosis remodeling is a key event in the development of heart anomalousness and dysfunction after myocardial infarction (MI). The purpose of this study was to explore the effect of activating transcription factor 3 (ATF3) on myocardial fibrosis remodeling after MI and its underlying mechanism, so as to provide a theoretical basis for the clinical development of new strategies for MI treatment., MI mouse formers were structured by hypodesmus of the left anterior descending (LAD) arteria coronaria of mice, and primary cardiac fibroblasts (CFs) were separated and cultivated to investigate the effect of ATF3 on myocardial fibrosis after MI and its mechanism., Increased collagen content and autophagic flux were found in the left ventricle (LV) tissues of MI mice as shown by Sirius red staining and Western blotting (WB) analysis. Meanwhile, immunofluorescence staining and WB analysis showed that ATF3 was raised in response to MI damage. After remedy with angiotensin II (AngII), the activity and differentiation of CFs were significantly raised, the expression of collagens was increased, and the level of autophagy was notably increased. Furthermore, AngII stimulation remarkably raised the expression of ATF3. Interestingly, knockdown of ATF3 in AngII-CFs reversed the above changes. In addition, after intervention with 3-methyladenine (3-MA), an autophagy restrainer, the activity and differentiation of AngII-CFs, as well as the relative collagen levels and autophagic flux were reduced. However, up-regulation of ATF3 protein expression partially reversed the effect of 3-MA on AngII-CFs., ATF3 can regulate the proliferation of CFs and collagen production by affecting autophagy, thus affecting myocardial fibrosis remodeling after MI.
资助项目Medical and Health Science and Technology Program of Zhejiang Province; [2023KY1154]
出版者ELSEVIER
ISSN0378-1119
EISSN1879-0038
卷号885
DOI10.1016/j.gene.2023.147705
页数8
WOS类目Genetics & Heredity
WOS研究方向Genetics & Heredity
WOS记录号WOS:001059387100001
收录类别PUBMED ; SCIE ; SCOPUS
在线发表日期2023-08
URL查看原文
PubMed ID37572799
SCOPUSEID2-s2.0-85167835592
通讯作者地址[Dai, Haiyue]Department of Cardiovascular Medicine,The Dingli Clinical College of Wenzhou Medical University,Laboratory of Wenzhou Pan Vascular Disease Management Center,252 Bailidong Road, Lucheng District, Zhejiang Province,Wenzhou,325000,China
Scopus学科分类Genetics
引用统计
文献类型期刊论文
条目标识符https://kms.wmu.edu.cn/handle/3ETUA0LF/182422
专题其他_定理临床学院(温州市中心医院)
通讯作者Dai, Haiyue
作者单位
Department of Cardiovascular Medicine,The Dingli Clinical College of Wenzhou Medical University,Laboratory of Wenzhou Pan Vascular Disease Management Center,Wenzhou,325000,China
第一作者单位其他_定理临床学院(温州市中心医院)
通讯作者单位其他_定理临床学院(温州市中心医院)
第一作者的第一单位其他_定理临床学院(温州市中心医院)
推荐引用方式
GB/T 7714
Huang, Yiwei,Dai, Haiyue. ATF3 affects myocardial fibrosis remodeling after myocardial infarction by regulating autophagy and its mechanism of action[J]. Gene,2023,885.
APA Huang, Yiwei, & Dai, Haiyue. (2023). ATF3 affects myocardial fibrosis remodeling after myocardial infarction by regulating autophagy and its mechanism of action. Gene, 885.
MLA Huang, Yiwei,et al."ATF3 affects myocardial fibrosis remodeling after myocardial infarction by regulating autophagy and its mechanism of action".Gene 885(2023).

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