Abstract
Diabetic cardiac myopathy (DCM) is a potent and independent risk factor in developing cardiovascular disease and heart failure. Despite successful management of comorbid cardiovascular risks, patients with diabetes still see increased incidents of heart failure. Hyperglycemia damages endothelial cells, causing inflammation and transcriptional derangement which drive endothelial cells to take on a mesenchymal phenotype, the process of EndMT. Cells with a mesenchymal phenotype then become a source of cardiac fibroblast-like cells that contribute to cardiac fibrosis, a defining characteristic of DCM.
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