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Dysregulation of circulating miRNAs promotes the pathogenesis of diabetes-induced cardiomyopathy

Authors :
Uzair Ahmed
Muhammad Qasim
Usman Ali Ashfaq
Muhammad Tariq
Saba Khaliq
Imtiaz Ahmad
Muhammad Shareef Masoud
Hafiz Usman Ahmad
Source :
PLoS ONE, Vol 16, Iss 4, p e0250773 (2021), PLoS ONE
Publication Year :
2021
Publisher :
Public Library of Science (PLoS), 2021.

Abstract

Diabetic Cardiomyopathy (DCM) is characterized by myocardial dysfunction caused by diabetes mellitus. After-effects of diabetic cardiomyopathy are far more lethal than non-diabetic cardiomyopathy. More than 300 million people suffer from diabetes and cardiovascular disorder which is expected to be elevated to an alarming figure of 450 million by 2030. Recent studies suggested that miRNA plays important role in the onset of diabetic cardiomyopathy. This study was designed to identify the miRNA that is responsible for the onset of diabetic cardiomyopathy using in silico and in vitro approaches. In this study, to identify the miRNA responsible for the onset of diabetic cardiomyopathy, in silico analysis was done to predict the role of these circulating miRNAs in type 2 diabetic cardiomyopathy. Shared miRNAs that are present in both diseases were selected for further analysis. Total RNA and miRNA were extracted from blood samples taken from type 2 diabetic patients as well as healthy controls to analyze the expression of important genes like AKT, VEGF, IGF, FGF1, ANGPT2 using Real-time PCR. The expression of ANGPT2 was up-regulated and AKT, VEGF, IGF, FGF1 were down-regulated in DCM patients as compared to healthy controls. The miRNA expression of miR-17 was up-regulated and miR-24, miR-150, miR-199a, miR-214, and miR-320a were down-regulated in the DCM patients as compared to healthy controls. This shows that dysregulation of target genes and miRNA may contribute towards the pathogenesis of DCM and more studies should be conducted to elucidate the role of circulating miRNAs to use them as therapeutic and diagnostic options.

Details

ISSN :
19326203
Volume :
16
Database :
OpenAIRE
Journal :
PLOS ONE
Accession number :
edsair.doi.dedup.....ed9002b37f225e9d0799ca337cf722bc