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miR-30a-5p inhibits the proliferation and collagen formation of cardiac fibroblasts in diabetic cardiomyopathy.

Authors:
Xiao-Xu Yang Zhen-Yu Zhao

Can J Physiol Pharmacol 2022 Feb 13;100(2):167-175. Epub 2022 Jan 13.

NHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin 300134, China.

Cardiac fibrosis is one of the major pathological characteristics of diabetic cardiomyopathy (DCM). MicroRNAs (miRNAs, miRs) have been identified as key regulators in the progression of cardiac fibrosis. This study aimed to investigate the role of in DCM and the underlying mechanism. The rat model of diabetes mellitus (DM) was established by streptozotocin injection, and the rat primary cardiac fibroblasts (CFs) were isolated from cardiac tissue and then treated with high glucose (HG). MTT assay was performed to assess the viability of CFs. Dual-luciferase reporter gene assay was conducted to verify the interaction between and . The expression of was downregulated in the myocardial tissues of DM rats and HG-stimulated CFs. Overexpression of reduced levels and inhibited collagen formation in HG-stimulated CFs and DM rats, as well as decreased the proliferation of CFs induced by HG. was a target of and its expression was inhibited by . Furthermore, the simultaneous overexpression of and reversed the effect of overexpression alone in CFs. Our results indicated that reduced expression and also induced a decrease in proliferation and collagen formation in DCM.

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http://dx.doi.org/10.1139/cjpp-2021-0280DOI Listing
February 2022

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