Date:2/15/2013

ity 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.

TITLE:
Diabetes increases mortality after myocardial infarction by oxidizing CaMKII

AUTHOR CONTACT:
Min Luo
University of Iowa Hospitals & Clinics, Iowa city, IA, USA
Phone: 319-356-2745; Fax: 319-356-8608; E-mail: min-luo-1@uiowa.edu

View this article at: http://www.jci.org/articles/view/65268?key=092be585f593debb00e1

ALSO IN THIS ISSUE

TITLE:
Depletion of FOXP3+ regulatory T cells promotes hypercholesterolemia and atherosclerosis

AUTHOR CONTACT:
Goran Hansson
Karolinska Institutet, Stockholm, SWE
Phone: 08-517-762-22; Fax: 46-8-313147; E-mail: Goran.Hansson@ki.se

View this ar
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Contact: Jillian Hurst press_releases@the-jci.org Journal of Clinical Investigation Source:Eurekalert

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