S14G-humanin confers cardioprotective effects against chronic adrenergic and pressure overload-induced heart failure in mice

作者全名："Zhao, Qi; Cai, Ming-Ming; Li, Dan; Zhao, Bin-Yi; Zhou, Shuang-Shan; Wu, Zhen-Ru; Shi, Yu-Jun; Su, Li"

作者地址："[Zhao, Qi; Cai, Ming-Ming; Li, Dan; Zhao, Bin-Yi; Zhou, Shuang-Shan; Su, Li] Chongqing Med Univ, Affiliated Hosp 2, Dept Cardiol, 288 Tianwen Ave, Chongqing 400010, Peoples R China; [Wu, Zhen-Ru; Shi, Yu-Jun] Sichuan Univ, West China Hosp, Lab Pathol, Chengdu 610041, Sichuan, Peoples R China"

通信作者："Su, L (通讯作者)，Chongqing Med Univ, Affiliated Hosp 2, Dept Cardiol, 288 Tianwen Ave, Chongqing 400010, Peoples R China."

来源：HELIYON

ESI学科分类：　

WOS号：WOS:001123642400001

JCR分区：Q1

影响因子：3.4

年份：2023

卷号：9

期号：11

开始页：　

结束页：　

文献类型：Article; Early Access

关键词：S14G-humanin; Heart failure; Cardiac remodeling; TGF-beta

摘要："S14G-humanin (HNG), an analog of the mitochondria-derived peptide humanin, has demonstrated protective effects against various cardiovascular diseases. However, the specific pharmacological effects of HNG in heart failure (HF) have not been previously reported. Therefore, in this study, we aimed to investigate the potential protective effect of HNG in HF using a mouse model. HF was induced in mice through intraperitoneal injection of isoproterenol or transverse aortic constriction, followed by separate administration of HNG to assess its therapeutic impact. Our results revealed that HNG treatment significantly delayed the onset of cardiac dysfunction and structural remodeling in the HF mouse model. Furthermore, HNG administration was associated with reduced infiltration of inflammatory cells, improved myocardial fibrosis, and attenuation of cardiomyocyte apoptosis in the treated cardiac tissues. Additionally, we identified the involvement of the transforming growth factor-beta signaling pathway in the beneficial effects of HNG in isoproterenol-induced HF mice. Collectively, these findings underscore the therapeutic potential of HNG in preventing the progression of HF, as demonstrated in two distinct HF mouse models."

基金机构：National Natural Science Foundation of China [NSFC 8197020688]

基金资助正文：<B>Funding</B> This work was supported by the National Natural Science Foundation of China (NSFC 8197020688) .