Karin Bornfeldt, Ph.D.
Professor, Departments of Medicine and Pathology
Associate Director, Diabetes & Obesity Center of Excellence
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 sub-optimal metabolic control and lipid abnormalities, such as increased levels of triglycerides and fatty acids, and decreased levels of HDL. Dr. Bornfeldt's research focuses on understanding the mechanisms of diabetes-accelerated atherosclerosis so that cardiovascular complications can be treated or prevented.
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 (About Dr. Ross). She also worked closely with Dr. Edwin Krebs on phosphorylation of signal transduction proteins in vascular cells (About Dr. Krebs). She was appointed to the faculty in 1995, and is now Professor of Pathology and serves as the Associate Director of the Diabetes and Obesity Center of Excellence.
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, Juvenile Diabetes Research Foundation, and the American Heart Association. She is a Fellow of the Council of Basic Cardiovascular Sciences, American Heart Association, and is a member of the editorial boards of the Journal of Clinical Investigation, Circulation Research, Diabetes, and the Journal of Biological Chemistry.
For additional information on Dr. Bornfeldt’s lab, please visit her lab website at http://www.pathology.washington.edu/research/labs/bornfeldt/.
Cellular and molecular mechanisms of diabetes-accelerated atherosclerosis. People with diabetes have an increased risk of developing cardiovascular complications caused by atherosclerosis, such as myocardial infarction, stroke and peripheral vascular disease. We use animal models and isolated vascular cells to investigate the processes that mediate diabetes-accelerated atherosclerosis. Projects range from in vivo studies to intracellular transduction studies.
Renard CB, Kramer F, Johansson F, Lamharzi N, Tannock LR, von Herrath MG, Chait A, Bornfeldt KE (2004): Diabetes and diabetes-associated lipid abnormalities have distinct effects on initiation and progression of atherosclerotic lesions. J Clin Invest. 114, 659-668.
Askari B, Kanter JE, Sherrid AM, Golej DL, Bender AT, Liu J, Hsueh WA, Beavo JA, Coleman RA & Bornfeldt KE (2007): Rosiglitazone inhibits acyl-CoA synthetase activity and fatty acid partitioning to diacylglycerol and triacylglycerol via a PPAR-independent mechanism in human arterial smooth muscle cells and macrophages. Diabetes. 56, 1143-1152.
Kanter JE, Johansson F, LeBoeuf RC & Bornfeldt KE (2007): Do glucose and lipids exert independent effects on atherosclerotic lesion initiation or progression to advanced plaques? Circ Res. 100, 769-781.
Johansson F, Kramer F, Barnhart S, Kanter JE, Vaisar T, Merrill RD, Geng L, Oka K, Chan L, Chait A, Heinecke JW & Bornfeldt KE (2008): Type 1 diabetes promotes disruption of advanced atherosclerotic lesions in LDL receptor-deficient mice. Proc Natl Acad Sci USA. 105, 2082-2087.
Li S, Sun Y, Liang CP, Thorp EB, Han S, Jehle AW, Saraswathi V, Pridgen B, Kanter JE, Li R, Welch CL, Hasty AH, Bornfeldt KE, Breslow JL, Tabas I & Tall AR (2009): Defective phagocytosis of apoptotic cells by macrophages in atherosclerotic lesions of ob/ob mice and reversal by a fish oil diet. Circ Res. 105, 1072-1082