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People with type 1 or type 2 diabetes have a greater risk of developing cardiovascular disease (myocardial infarction, stroke, and peripheral cardiovascular disease that can lead to the necessity to amputate limbs) caused by atherosclerosis. These complications also develop earlier in life than in people without diabetes. Risk factors for cardiovascular disease associated with diabetes include sub-optimal metabolic control and lipid abnormalities, such as increased levels of triglycerides and decreased levels of HDL. Our work focuses on understanding the mechanisms of diabetes-accelerated atherosclerosis so that these complications can be treated or prevented.

We have shown, using a mouse model of diabetes-accelerated atherosclerosis (Renard et al. 2004; Johansson et al. 2008) that type 1 diabetes stimulates both initiation of lesions of atherosclerosis and progression to advanced lesions. Our working hypothesis is that diabetes stimulates lesion initiation and progression by increasing macrophage recruitment and arterial inflammation.

Our work is, or has been, funded by the National Heart, Lung, and Blood Institute, the American Heart Association, the American Diabetes Association, Seattle Foundation, the Royalty Research Fund at the University of Washington, and the Juvenile Diabetes Research Foundation.