详情页 - 聚合机构库演示平台

当前位置：首页 > 详情页

CD9 exacerbates pathological cardiac hypertrophy through regulating GP130/STAT3 signaling pathway

57| 导出 | 链接全文 |

文献详情

资源类型：

WOS体系：

Pubmed体系：

收录情况： ◇ SCIE

作者：

单位： [1]Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China. [2]Gene Hospital of Henan Province, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China. [3]Cardiovascular Center, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, China. [4]Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China. [5]Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, China. [6]Institute of Pathology,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan,Hubei 430030,China. [7]Department of Gastrointestinal Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China.

出处：

DOI：

ISSN：

摘要：

CD9 is a member of the tetraspanin protein family, which has been widely studied in inflammation and cancer, but not in pathological cardiac hypertrophy. In this study, we found that the expression of CD9 was increased in transaortic constriction (TAC) myocardial tissue. Knockdown of CD9 alleviated damage to cardiac function in the TAC model and reduced heart weight, cardiomyocyte size, and degree of fibrosis, and vice versa. Mechanistically, co-immunoprecipitation results showed that CD9 and GP130 can bind to each other in cardiomyocytes, and knockdown of CD9 can reduce the protein level of GP130 and the phosphorylation of STAT3 in vivo and in vitro, and vice versa. GP130 knockdown reversed the aggravating effects of CD9 on pathological cardiac hypertrophy. Therefore, we conclude that CD9 exacerbates pathological cardiac hypertrophy by regulating the GP130/STAT3 signaling pathway and may serve as a therapeutic target for pathological cardiac hypertrophy.© 2023 The Authors.

基金：

语种：

WOS：

PubmedID：

中科院(CAS)分区：

出版当年[2022]版：

大类 | 2 区综合性期刊

小类 | 2 区综合性期刊

最新[2025]版：

大类 | 2 区综合性期刊

小类 | 2 区综合性期刊

JCR分区：

出版当年[2021]版：

Q1 MULTIDISCIPLINARY SCIENCES

最新[2023]版：

Q1 MULTIDISCIPLINARY SCIENCES

影响因子： 4.6 最新[2023版] 5 最新五年平均 6.107 出版当年[2021版] 6.233 出版当年五年平均 5.458 出版前一年[2020版] 5.8 出版后一年[2022版]

第一作者：

第一作者单位： [1]Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China. [2]Gene Hospital of Henan Province, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China.

共同第一作者：

通讯作者：

通讯机构： [2]Gene Hospital of Henan Province, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China. [7]Department of Gastrointestinal Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China.

推荐引用方式(GB/T 7714)：

APA：

MLA：