Karin Bornfeldt received her PhD from Linköping University in Sweden in 1991. Later that year, she came to the University of Washington to do a postdoctoral fellowship in the laboratory of Dr. Russell Ross, a leader in the field of cardiovascular medicine. She also worked closely with Dr. Edwin Krebs on phosphorylation of signal transduction proteins in vascular cells. She was appointed to the faculty in 1995, and is now Professor of Medicine and Pathology and serves as the Associate Director of the Diabetes and Obesity Center of Excellence and Deputy Director of the Diabetes Research Center.
Dr. Bornfeldt is actively involved in graduate student teaching and has served on more than 20 Doctoral Supervisory Committees in Pathology, Molecular and Cellular Biology, Pharmacology, and Nutritional Sciences.
Dr. Bornfeldt frequently serves on study sections on cardiovascular biology and the complications of diabetes at the NIH and the American Heart Association. She is a Fellow of the Council of Basic Cardiovascular Sciences, American Heart Association, is Consulting Editor for Arteriosclerosis, Thrombosis and Vascular Biology, Associate Editor for Circulation Research, and is or has been a member of the editorial boards of the Journal of Clinical Investigation, Circulation Research, Diabetes, and the Journal of Biological Chemistry.
People with type 1 or type 2 diabetes/insulin resistance have a greater risk of developing cardiovascular disease (myocardial infarction, stroke, and peripheral cardiovascular disease that can lead to the necessity to amputate limbs). The cardiovascular disease is caused primarily by atherosclerosis. These cardiovascular complications also develop earlier in life compared to people without diabetes. Risk factors for cardiovascular disease associated with diabetes include inflammatory changes, sub-optimal metabolic control and lipid abnormalities, such as increased levels of triglycerides and fatty acids, and decreased levels of HDL cholesterol. Dr. Bornfeldt’s research focuses on understanding the mechanisms of diabetes-accelerated atherosclerosis so that cardiovascular complications can be treated or prevented.
Dr. Bornfeldt’s laboratory has shown, using a mouse model of type 1 diabetes-accelerated atherosclerosis, that diabetes stimulates both initiation of lesions of atherosclerosis and progression to advanced lesions. The working hypothesis is that diabetes stimulates lesion initiation and progression by increasing recruitment of inflammatory cells and arterial inflammation.
More resent research by Dr. Bornfeldt’s group has identified a key step in the mechanism of diabetes-induced inflammatory changes and atherosclerosis. The culprit, acyl-CoA synthetase 1, is an enzyme that converts free fatty acids into their acyl-CoA derivatives in myeloid cells. Current research focuses on the role glucose and acyl-CoAs might play in endothelial dysfunction, inflammation and diabetes-accelerated atherosclerosis. Dr. Bornfeldt is also interested in other inflammatory biomarkers and mediators in relation to both type 1 and type 2 diabetes, and insulin resistance.
