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Additionally, experimental studies have shown that cardiac glycolipid toxicity, impaired insulin signaling, cardiac energetic impairment, activation of the reninangiotensin system (RAS) and increased formation of angiotensin II (Ang II), cardiac autonomic neuropathy, reduced NO bioavailability, elevations in AGEs, and dysregulated cardiomyocyte calcium handling, play central roles in diabetic cardiomyopathy pathologies (Figure 1) (Pechnov et al., 2015

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PMID 19178874