C1q/TNF-related protein 3 alleviates heart failure via attenuation of oxidative stress in myocardial infarction rats

被引：5

作者：

Liu, Yu ^{[1
]}

Wu, Pinxia ^{[2
]}

Xu, Xiaohong ^{[1
]}

Shen, Tongtong ^{[1
]}

Wang, Xinxin ^{[1
]}

Liu, Yayuan ^{[1
]}

Yuan, Chen ^{[1
]}

Wang, Tian ^{[1
]}

Zhou, Limin ^{[1
]}

Liu, Ai ^{[3
,4
]}

机构：

[1] Anhui Med Univ, Dept Internal Med, Div Cardiol, Affiliated Chuzhou Hosp, Chuzhou City, Anhui Province, Peoples R China

[2] Anhui Med Univ, Dept Rehabil Med, Affiliated Chuzhou Hosp, Chuzhou City, Anhui Province, Peoples R China

[3] ChuZhou City Vocat Coll, Chuzhou City, Anhui Province, Peoples R China

[4] Chuzhou City Career Acad, 101 Zuiweng Rd, Chuzhou City 239000, Anhui Province, Peoples R China

来源：

PEPTIDES | 2023年 / 163卷

关键词：

Heart failure; Myocardial infarction; Fibrosis; C1q-tumor necrosis factor-related protein-3; Oxidative stress; CARDIAC DYSFUNCTION; CELL-DEATH; CTRP3; INFLAMMATION;

D O I：

10.1016/j.peptides.2023.170980

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

C1q-tumor necrosis factor-related protein 3 (CTRP3), an adipokine, has been reported to be closely related to cardiovascular diseases (CVDs). However, the effect of CTRP3 on heart failure (HF) remains dimness. This study was to explore the role of CTRP3 in HF and its potential interaction mechanism. Heart failure model was established by inducing ischemia myocardial infarction (MI) through ligation of the left anterior descending artery in Sprague-Dawley rats. Four weeks later, the rats were detected by transthoracic echocardiography and masson staining. Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), cardiac troponin I (cTnI) levels, creatine kinase-MB (CK-MB) and oxidative stress levels were recorded. The level of CTRP3 was reduced in the cardiomyocytes (CMs) treated with oxygen-glucose deprivation (OGD) and in the heart of MI rats. CTRP3 overexpression alleviated cardiac dysfunction, attenuated the cardiac fibrosis, and inhibited the increases of ANP, BNP, cTnI and CK-MB in the serum of MI rats. The increases of ANP and BNP in the CMs, and the collagen I and collagen III in the cardiac fibroblasts (CFs) induced by OGD were inhibited by CTRP3 overexpression. The enhancement of oxidative stress in the heart of MI rats was inhibited by CTRP3 overexpression. These results indicated that overexpression of CTRP3 could improve cardiac function and the related cardiac fibrosis in MI-induced HF rats via inhibition of oxidative stress. Upregulation of CTRP3 may be a strategy for HF therapy in the future.

引用

页数：7