Fig. 1From: Current status and strategies of long noncoding RNA research for diabetic cardiomyopathyPathogenesis of diabetic cardiomyopathy. In diabetes mellitus, repressed glucose oxidation, enhanced fatty acid metabolism, hyperinsulinemia, insulin resistance, and accumulation of advanced glycation end-products lead to oxidative stress, microcirculation impairment, mitochondrial dysfunction, and autonomic neuropathy. These pathogenic factors together result in myocardial inflammation, endothelial dysfunction, necrosis, apoptosis, autophagy, fibrosis, athrosclerosis, and cardiac hypertrophy, impair Ca2+ homeostasis, and activate the renin-angiotensin system (RAS). Eventually these pathogenic changes in the myocardium impair the diastolic and systolic function of the heartBack to article page