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Diabetic cardiomyopathy (DCM) is an independent clinical entity defined as structural and functional changes in the myocardium because of metabolic and cellular abnormalities induced by diabetes, resulting in cardiac failure. Hyperglycemia has been seen as a major cause of DCM due to activation of different mechanisms leading to oxidative stress. Several body of evidence show that distinct pathways of oxygen and nitrogen reactive species formation contribute to myocardial impairment. Abnormal mitochondrial morphology and energetics, evoked by abnormal Ca2+ handling, metabolic changes and oxidative stress, are observed in DCM, suggesting a pivotal role of mitochondrial dynamics in disease pathogenesis. In addition, insulin resistance compromises myocardial glucose uptake due to cellular depletion of glucose transporter proteins, together with increased myocardial uptake of free fatty acids and augmented triglyceride levels, which cause cardiomyocyte lipotoxicity. Finally, the state of chronic low-grade inflammation, a feature of obese type 2 diabetes, seems to also play a major role in DCM progression, whose mechanisms have been progressively disclosed. In this book chapter, we review the cellular mechanism contributing to DCM development, focusing on oxidative stress, mitochondrial dysfunction and inflammation of cardiomyocytes, as well as on possible therapeutic strategies.

Diabetic Cardiomyopathy: Focus on Oxidative Stress, Mitochondrial Dysfunction and Inflammation