Molecular Basis of Cardiomyopathies in Type 2 Diabetes

Figures

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  Figure 1. The link between apoptosis, autophagy, pyro-apoptosis, and cardiomyocyte loss in DbCM, inflammation and metabolic stress contribute to the senescence of cardiomyocytes. AGEs: advanced glycation end products; DbCM: diabetic cardiomyopathy; ERS: stress endoplasmic reticulum; ROS: reactive oxygen species.

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  Figure 2. Molecular mechanisms involved in the development of DbCM: accumulation of FAs contributes to mitochondrial dysfunction with increased production of ROS and consequent oxidative stress in cardiomyocytes. This causes a higher rate of apoptosis, which is also enhanced by inflammation that is sustained by the production of cytokines. Cytokines are released through the activation of NF-kB, which is mainly sustained by hyperglycemia, the accumulation of AGEs and the activation of their receptor AGE. Other contributing mechanisms are the disarrangement of RAAS, the stress on ER and epigenetics, which is induced by hyperglycemia and hyperinsulinism, which contribute to modification of the gene expression and cellular phenotype. The principal perturbations in the heart are fibrosis, cardiac hypertrophy and diastolic dysfunction, which are all main features of DbCM. AGE: advanced glycation end product; DbCM: diabetic cardiomyopathy; ER: endoplasmic reticulum; FAs: fatty acids; RAAS: renin angiotensin aldosterone system; ROS: reactive oxygen species.