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Targeting miRNA for Therapy of Juvenile and Adult Diabetic Cardiomyopathy

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Exosomes, Stem Cells and MicroRNA

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 1056))

Abstract

Prevalence of diabetes mellitus (DM), a multifactorial disease often diagnosed with high blood glucose levels, is rapidly increasing in the world. Association of DM with multi-organ dysfunction including cardiomyopathy makes it a leading cause of morbidity and mortality. There are two major types of DM: type 1 DM (T1D) and type 2 DM (T2D). T1D is diagnosed by reduced levels of insulin and high levels of glucose in the blood. It is caused due to pancreatic beta cell destruction/loss, and mostly found in juveniles (juvenile DM). T2D is diagnosed by increased levels of insulin and glucose in the blood. It is caused due to insulin receptor dysfunction, and mostly found in the adults (adult DM). Both T1D and T2D impair cardiac muscle function, which is referred to as diabetic cardiomyopathy. We and others have reported that miRNAs, a novel class of tiny non-coding regulatory RNAs, are differentially expressed in the diabetic heart and they contribute to diabetic cardiomyopathy. Here, we elaborated the biogenesis of miRNA, how miRNA regulates a gene, cardioprotective roles of different miRNAs including miRNAs present in exosomes, underlying molecular mechanisms by which miRNA ameliorates diabetic cardiomyopathy, and the role of miRNA as a potential therapeutic target for juvenile and adult diabetic cardiomyopathy.

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Acknowledgements

This work was supported in part by American Heart Association Postdoctoral fellowship award 16POST30180003 to S.S.N., and the National Institutes of Health grants HL-113281 and HL-116205 to P.K.M.

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Correspondence to Paras Kumar Mishra .

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Nandi, S.S., Mishra, P.K. (2018). Targeting miRNA for Therapy of Juvenile and Adult Diabetic Cardiomyopathy. In: Mettinger, K., Rameshwar, P., Kumar, V. (eds) Exosomes, Stem Cells and MicroRNA. Advances in Experimental Medicine and Biology, vol 1056. Springer, Cham. https://doi.org/10.1007/978-3-319-74470-4_4

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