败血症
炎症
细胞凋亡
生物
脂多糖
射血分数
舒张期
下调和上调
内科学
血压
肿瘤坏死因子α
免疫学
心脏病学
癌症研究
内分泌学
医学
心力衰竭
生物化学
基因
作者
Lan Gao,Zhongjie Zhai,Qiong Shi,Jin Yan,Linjing Zhou,Yongxin Wu,Qinjing Zeng,Gang Tian,Hao Li
出处
期刊:Cell Cycle
[Informa]
日期:2022-03-01
卷期号:21 (9): 961-971
被引量:1
标识
DOI:10.1080/15384101.2022.2035618
摘要
Sepsis-induced myocardial dysfunction is a common complication in septic patients. To date, a limited number of biomarkers that could predict cardiomyocyte apoptosis have been explored. In this study, we successfully established a cecal ligation and puncture (CLP)-induced septic model, and it was found that miR-501-5p expression was down-regulated in peripheral blood samples of septic patients with cardiac dysfunction, lipopolysaccharide (LPS)-induced cardiomyocytes, and the myocardium and peripheral blood in the septic model. Moreover, it was revealed that miR-501-5p overexpression could increase left ventricular diastolic pressure (LVDP), fractional shortening (FS), ejection fraction (EF), and maximum rate of the rise of left ventricular pressure (+dp/dt) in vivo, while it decreased the levels of myocardial injury-related indicators. In addition, LPS induction accelerated apoptosis and elevated the inflammation in HL-1 and HCM cells, which could be reversed by miR-501-5p overexpression. Mechanistically, we considered nuclear receptor subfamily 4 group A member 3 (NR4A3) as the target of miR-501-5p, and it was found that miR-501-5p prevented the binding between NR4A3 and Bcl-2. It was found that miR-501-5p exerted an inhibitory effect on cardiomyocyte apoptosis and inflammation in a NR4A3-dependent manner. Overall, our results may provide evidence for consideration of miR-501-5p in the therapy of sepsis.
科研通智能强力驱动
Strongly Powered by AbleSci AI