Diabetic Cardiomyopathy: An Update of Mechanisms Contributing to This Clinical Entity

Diabetic Cardiomyopathy: An Update of Mechanisms Contributing to This Clinical Entity

Guanghong Jia, Michael A. Hill, James R. Sowers

The molecular proteins and signaling pathways in hyperglycemia- and insulin resistance-diabetic cardiomyopathy. Increased protein kinase C (PKC), mitogen-activated protein kinase (MAPK), nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB), sodium–glucose cotransporter-2 (SGLT2), O-linked N-acetylglucosamine (O-GlcNAc), and cyclic adenosine 5’-monophosphate-responsive element modulator (CREM) signaling, dysregulation of microRNA (miRNA) and exosomes, and reduction of AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor (PPAR)-γ, and nuclear factor erythroid 2–related factor 2 (Nrf2) induce cardiac insulin resistance, subcellular component abnormalities, metabolic disorders, and structural changes, resulting in diabetic cardiomyopathy. [Powerpoint FIle]

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