糖尿病性心肌病
基因沉默
糖尿病
内科学
医学
程序性细胞死亡
猝死
下调和上调
心力衰竭
心肌细胞
心肌病
内分泌学
细胞生物学
心脏病学
生物
基因
生物化学
细胞凋亡
作者
Chao Shi,Lifang Wu,Ling Li
出处
期刊:Cellular and Molecular Biology
日期:2022-02-27
卷期号:67 (6): 213-219
被引量:2
标识
DOI:10.14715/cmb/2021.67.6.28
摘要
Diabetic cardiomyopathy (DCM) is a common complication of diabetes mellitus, often leading to heart failure, arrhythmias and sudden death. Long-stranded non-coding RNA (LncRNA), an endogenous non-coding long-stranded RNA, is associated with diabetic cardiomyopathy. However, the mechanism of LncRNA regulation of cellular scorching in diabetic cardiomyopathy remains unclear. This study aimed to elucidate whether MALAT 1 affects cardiomyocyte scorching in DCM patients.Streptozotocin (STZ) at 35 mg/Kg was used to induce diabetes in rats. H9C2 cardiomyocytes and primary cardiomyocytes (PCM) were cultured at 5.5 and 50 mmol/L glucose, respectively. The expression levels of MALAT 1 and scorch death-related genes were detected by RT-PCR using plasmids to suppress or overexpress the related genes, respectively. Immunofluorescence, RT-PCR and Western blot were used to detect the extent of cell scorch death.MALAT 1 expression was elevated in diabetic and high glucose-induced cardiomyocytes and myocardial tissue from diabetic mice (p<0.001). Silencing of MALAT 1 alleviated cardiomyocyte scorch death by targeting NLRP3. Furthermore, silencing MALAT 1 reduced cell death and improved cardiac function and morphology.MALAT 1 is overexpressed in DCM and silencing MALAT 1 inhibits cell scorch death by affecting NLRP3 expression. We clarify for the first time that MALAT 1 may be a new therapeutic target for DCM.
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