MiR-410-5p promotes the development of diabetic cardiomyopathy by suppressing PIM1-induced anti-apoptosis. (August 2020)

• Record Type: Journal Article
• Authors: Xia, Xiaofen; Liang, Yan; Zheng, Weihong; Lin, Dongming; Sun, Shuping
• Is Part Of: Molecular and cellular probes. Volume 52(2020)
• Publication Date: 2020-08
• Subjects: Diabetic cardiomyopathy -- miR-410-5p -- PIM1 -- Apoptosis; Molecular probes -- Diagnostic use -- Periodicals; Pathology, Cellular -- Technique -- Periodicals; Cell Biology -- Periodicals; Molecular Biology -- Periodicals; Sondes moléculaires -- Utilisation diagnostique -- Périodiques; Cytopathologie -- Technique -- Périodiques; 572
• DOI: 10.1016/j.mcp.2020.101558
• Languages: English
• ISSNs: 0890-8508

Abstract

Abstract: Diabetic cardiomyopathy (DCM) is a common complication of diabetes mellitus that can cause many severe symptoms, such as heart failure, arrhythmia, and sudden death. However, the molecular mechanisms underlying cardiac dysfunction in DCM remain elusive. In this study, we found that miR-410-5p was increased in the myocardial tissue of a diabetes mellitus (DM) rat model. Further studies confirmed that inhibition of miR-410-5p reduced cell apoptosis by regulating the Bcl-2/Bax axis. Through bioinformatics analysis and luciferase reporter assays, we observed that miR-410-5p directly targets PIM1. Moreover, knockdown of miR-410-5p by antagomir-410-5p improved diabetes-induced cardiac function and myocardial tissue structure. In conclusion, our study demonstrated that miR-410-5p might be involved in the progression of DCM by targeting PIM1 and might be a promising therapeutic target for DCM in the future. Highlights: miR-410-5p was increased and regulates myocardial apoptosis a in DCM. miR-410-5p contributes to the progression of DCM was demonstrated in this test. The regulatory network between miR-410-5p and PIM1 may provide new insights in the treatment of DCM.