Diabetic patients are more than twice as likely to die from a heart attack as non-diabetic patients, but the mechanisms that underlie increased heart attack-related mortality in diabetic patients are unknown. High levels of the oxidized form of the protein CamKII (ox-CaMKII) have been linked to increased risk of sudden death after heart attack. Additionally, hearts from diabetic patients have significantly greater ox-CAMKII compared to hearts from non-diabetic patients. In this issue of the Journal of Clinical Investigation, Min Luo and colleagues at the University of Iowa used a mouse model of diabetest to determine if ox-CAMKII was an essential component of the molecular pathway that increases heart attack-related mortality in diabetic patients. The transgenic mouse model was engineered to express a form of CaMKII that cannot be oxidized in the heart muscle. Luo and colleagues found that diabetic mice expressed the non-oxidizable form of CamKII were less likely to die after a heart attack than mice that expressed normal CamKII. These findings suggest that ox-CAMKII may also increase post-heart attack mortality in diabetic patients and indicate that therapies that reduce oxidation of CamKII could be useful in treating diabetic patients who suffer from cardiovascular disease.
Diabetes increases mortality after myocardial infarction by oxidizing CaMKII
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