Abstract
Diabetes mellitus (DM) is on the rise, necessitating the development of novel therapeutic and preventive strategies to mitigate the disease's debilitating effects. Diabetic cardiomyopathy (DCMP) is among the leading causes of morbidity and mortality in diabetic patients globally. DCMP manifests as cardiomyocyte hypertrophy, apoptosis, and myocardial interstitial fibrosis before progressing to heart failure. Evidence suggests that non-coding RNAs, such as long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), regulate diabetic cardiomyopathy-related processes such as insulin resistance, cardiomyocyte apoptosis and inflammation, emphasizing their heart-protective effects. This paper reviewed the literature data from animal and human studies on the non-trivial roles of miRNAs and lncRNAs in the context of DCMP in diabetes and demonstrated their future potential in DCMP treatment in diabetic patients.
Keywords:
cardiomyopathy; diabetes; long non-coding RNAs; microRNAs; therapeutic application.
Copyright © 2023 Macvanin, Gluvic, Radovanovic, Essack, Gao and Isenovic.
Publication types
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Review
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Deoxycytidine Monophosphate
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Diabetes Mellitus* / pathology
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Diabetic Cardiomyopathies* / pathology
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Fibrosis
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Humans
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MicroRNAs* / genetics
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Myocardium / pathology
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RNA, Long Noncoding* / genetics
Substances
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MicroRNAs
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RNA, Long Noncoding
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Deoxycytidine Monophosphate
Grants and funding
This work is part of the collaboration between the Department of Radiobiology and Molecular Genetics, “VINČA” Institute of Nuclear Sciences - National Institute of the Republic of Serbia, University of Belgrade, Belgrade, Serbia, Clinic for Internal Medicine, Department of Endocrinology and Diabetes, Zemun Clinical Hospital, School of Medicine, University of Belgrade, Belgrade, Serbia, and KAUST. The research was funded by the Ministry of Education, Science and Technological Development of the Republic of Serbia (Contract No# 451-03-47/2023-01/200017) and King Abdullah University of Science and Technology (KAUST) through grant awards Nos. BAS/1/1624-01-01, FCC/1/1976-20-01, FCC/1/1976-26-01, and Contract No#OSR 4129.