Cardiovascular disease represents the major cause of morbidity and mortality in patients with diabetes mellitus.
Studies by us and others have implicated increased flux via aldose reductase (AR) as a key player in mediating diabetic
complications, including cardiovascular complications. Data suggest that increased flux via AR in diabetics perpetuates
increased injury after myocardial infarction, accelerates atherosclerotic lesion formation, and promotes restenosis via
multiple mechanisms. Most importantly, studies have shown that increased generation of reactive oxygen species due to
flux via AR has been a common feature in animal models of diabetic cardiovascular disease. Taken together, these
considerations place AR in the center of biochemical and molecular stresses that characterize the cardiovascular
complications of diabetes. Stopping AR-dependent signaling may hold the key to interrupting cycles of cellular
perturbation and tissue damage in diabetic cardiovascular complications.
Keywords: Advanced glycation end products, Aldose reductase, Aldose reductase inhibitors, atherosclerosis, cardiovascular
complications, Diabetes, hyperglycemia, ischemia reperfusion, Oxidative stress, Polyol pathway
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