4.5 Article

Integrated analysis of mRNA and microRNA expression profiles reveals differential transcriptome signature in ischaemic and dilated cardiomyopathy induced heart failure

Journal

EPIGENETICS
Volume 16, Issue 8, Pages 917-932

Publisher

TAYLOR & FRANCIS INC
DOI: 10.1080/15592294.2020.1827721

Keywords

Heart failure; gene expression; microRNA; miRNA-mRNA network; cardiac remodelling

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Cardiac remodelling is a common characteristic of heart diseases, especially heart failure. MicroRNA and mRNA are potential diagnostic markers and therapeutic targets for heart failure. MicroRNA-mRNA interaction network analysis identified miR-542-3p-CILP as a potential new mechanism in ischaemic cardiomyopathy-induced heart failure.
Cardiac remodelling is widely accepted as a common characteristic for many heart diseases, especially in heart failure (HF). Ischaemic cardiomyopathy (ICM) and dilated cardiomyopathy (DCM) are associated with cardiac remodelling. Both mRNA and microRNA are potential diagnostic markers and therapeutic targets of cardiac remodelling in HF. However, the mechanisms of microRNA-mRNA joint regulation in HF are still unclear. In this study, 3 gene expression profiles from patients with and without HF were analysed to harvest shared differentially expressed genes (microRNA and mRNA) with significant major biological function. Moreover, key genes highly related to ICM and DCM-induced HF were screened out through a Weighted Genes Co-Expression Network Analysis (WGCNA). Based on microRNA-mRNA analysis, several microRNAs and target genes were identified. Combined with pathway analysis, we found that miR-542-3p and its target gene CILP were likely involved in the regulation of TGF-beta signalling pathway in ICM induced HF. Collectively, the microRNA-mRNA interaction network analysis revealed that miR-542-3p-CILP as mediator of TGF-beta signalling pathway might be a new mechanism to mediate ICM induced HF. This study provides certain novel targets for diagnosis and therapeutic treatment of ICM- and DCM-induced HF.

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