Figure 1.

Oxidative stress, inflammation, alterations in metabolic pathways (including abnormalities in substrate utilization, mitochondrial function, advanced glycation end-product [AGE] formation and O-GlcNAcylation), as well as changes at the level of insulin signaling, gene regulation, endoplasmic reticulum (ER) stress, neurohumoral activation and cardiac cell death, have all been widely accepted as mediators of diabetes-induced myocardial remodeling and dysfunction (see text for references).