Diabetic cardiomyopathy

Definition:

Diabetic cardiomyopathy has been defined as left ventricular dysfunction that occurs among patients with diabetes mellitus independent of a recognized cause such as coronary artery disease or hypertension. The pathogenesis of diabetic cardiomyopathy broadly involves hyperglycemia, increased circulating fatty acids, and insulin resistance contributing to reactive oxygen species (ROS) generation, mitochondrial dysfunction, impaired calcium metabolism, Renin-Angiotensin System (RAS) activation, and altered substrate metabolism. These effects result in cardiac fibrosis, hypertrophy, cardiomyocyte death, contractile dysfunction, endothelial cell damage and eventually heart failure. In the process of cardiac fibrosis, cardiac fibroblasts are the final effector cell.

References:

[1]. Guanghong Jia, et al. Insulin resistance and hyperinsulinaemia in diabetic cardiomyopathy. Nat Rev Endocrinol. 2016 Mar;12(3):144-53. [Content Brief]

[2]. Mandip Joshi, et al. Conundrum of pathogenesis of diabetic cardiomyopathy: role of vascular endothelial dysfunction, reactive oxygen species, and mitochondria. Mol Cell Biochem. 2014 Jan;386(1-2):233-49. [Content Brief]

[3]. Scott P Levick, et al. The Diabetic Cardiac Fibroblast: Mechanisms Underlying Phenotype and Function. Int J Mol Sci. 2020 Feb 1;21(3):970. [Content Brief]

[4]. U Varma, et al. Molecular mechanisms of cardiac pathology in diabetes - Experimental insights. Biochim Biophys Acta Mol Basis Dis. 2018 May;1864(5 Pt B):1949-1959. [Content Brief]

[5]. Xavier Palomer, et al. Emerging Actors in Diabetic Cardiomyopathy: Heartbreaker Biomarkers or Therapeutic Targets?. Trends Pharmacol Sci. 2018 May;39(5):452-467. [Content Brief]

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