Abstract
Diabetic cardiomyopathy (DMCM) is the leading cause of mortality and morbidity among diabetic patients. DMCM is characterized by an increase in oxidative stress with systemic inflammation that leads to cardiac fibrosis, ultimately causing diastolic and systolic dysfunction. Even though DMCM pathophysiology is well studied, the approach to limit this condition is not met with success. This highlights the need for more knowledge of underlying mechanisms and innovative therapies. In this regard, emerging evidence suggests a potential role of non-coding RNAs (ncRNAs), including micro-RNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) as novel diagnostics, mechanisms, and therapeutics in the context of DMCM. However, our understanding of ncRNAs’ role in diabetic heart disease is still in its infancy. This review provides a comprehensive update on pre-clinical and clinical studies that might develop therapeutic strategies to limit/prevent DMCM.
Highlights
This review focuses on the role of micro-RNAs, long non-coding RNAs (lncRNAs), and circular RNAs in the DMCM (Figure 2 and Table 3)
A recent study performed on myocardial microvascular endothelial cells (MMECs) from type 2 diabetes mellitus (T2DM) Goto-Kakizaki rats showed that miRNA-193-5p plays an important role as an angiogenic factor in DMCM by negatively regulating the expression of insulin growth factor2 (IGF-2) (Yi et al, 2017)
Need to be addressed: (a) robust computational techniques for their identification and downstream targets should be standardized, (b) novel regulatory mechanisms need to be uncovered, (c) it should be investigated if lncRNA translation products proteins/peptides are functional, and (d) genetic models of lncRNA should be established
Summary
Another study by Feng et al (2010) performed on STZ-induced T1DM mouse models demonstrated significantly reduced levels of miR-133a in cardiac tissue. Recent findings by Tao et al (2020) reveal the role of miR-144 in the protection of the diabetic heart by regulating cardiomyocyte apoptosis, displaying that miR-144 was found to be significantly decreased in HGtreated cardiomyocytes and in the heart of STZ-induced diabetic mice, which were associated with mitochondrial dysfunction and cell death.
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