Open AccessConstruction and analysis of a lncRNA‑miRNA‑mRNA network based on competitive endogenous RNA reveals functional lncRNAs in diabetic cardiomyopathy
Author(s) -
Kai Chen,
Yunci Ma,
Shaoyu Wu,
Yuxin Zhuang,
Xin Liu,
LiangChuan Lin,
Guohua Zhang
Publication year - 2019
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2019.10361
Subject(s) - competing endogenous rna , xist , microrna , biology , long non coding rna , computational biology , diabetic cardiomyopathy , rna , messenger rna , gene regulatory network , bioinformatics , gene , gene expression , genetics , cardiomyopathy , heart failure , medicine , x inactivation , x chromosome
Diabetic cardiomyopathy (DCM) is a major cause of mortality in patients with diabetes, particularly those with type 2 diabetes. Long non‑coding RNAs (lncRNAs), including terminal differentiation‑induced lncRNA (TINCR), myocardial infarction‑associated transcript (MIAT) and H19, serve a key role in the regulation of DCM. MicroRNAs (miRNAs/miRs) can inhibit the expression of mRNA at the post‑transcriptional level, whereas lncRNAs can mask the inhibitory effects of miRNAs on mRNA. Together, miRNAs and lncRNAs form a competitive endogenous non‑coding RNA (ceRNA) network that regulates the occurrence and development of various diseases. However, the regulatory role of lncRNAs in DCM is unclear. In this study, a background network containing mRNAs, miRNAs and lncRNAs was constructed using starBase and a regulatory network of DCM was screened using Cytoscape. A functional lncRNA, X‑inactive specific transcript (XIST), was identified in the disease network and the main miRNAs (miR‑424‑5p and miR‑497‑5p) that are regulated by XIST were further screened to obtain the ceRNA regulatory network of DCM. In conclusion, the results of this study revealed that lncRNAs may serve an important role in DCM and provided novel insights into the pathogenesis of DCM.