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.
