“…The known mechanisms and pathways involved in early cardiomyocytic damage and subsequent aggravation are metabolic disturbances (decreased glucose oxidation, increased free fatty acids), impaired cellular function (inadequate calcium handling, augmented oxidative stress, mitochondrial dysfunction), structural alterations (advanced glycation end-product, cardiomyocyte hypertrophy), in addition to the activation of the renin-angiotensin-aldosterone system (fibrosis and cardiomyocyte stiffness) and cardiac autonomic neuropathy. These are triggered by hyperglycemic and lipotoxic anomalies related to insulin resistance, the prominent feature in type 2 diabetes [21,22,23,24,25,26,27,28,29,30]. Figure 2 summarizes the cellular, structural, and functional anomalies, the main imaging features, and the serological biomarkers involved in the earlier stages of diabetic cardiomyopathy [23,25,31,32,33,34,35,36,37].…”