What are the molecular mechanisms that results in complications of diabetes?
Diabetes is increasing as a result of increased rates of obesity, and with that complications of diabetes are also on the rise. These include diabetic kidney disease and macrovascular complications such as cardiovascular disease due to underlying atherosclerosis. In the laboratory we are focused on these two main complications of diabetes, and how they potentially interact. We are especially interested in myeloid cells (monocytes and macrophages), and how they get activated under diabetic conditions and their role in acceleration of diabetes-associated complications, such as kidney disease. The laboratory has recently generated a model to study the combination of diabetic kidney disease and atherosclerosis. This will allow us to ask what molecular mechanisms drive the individual complications but also the interaction between them. One of these mechanisms appear to be augmented inflammatory signals, perhaps driven by diabetic dyslipidemia.
Another project in the laboratory is focused on investigating why diabetic are more likely to have another myocardial infarction after suffering the first one. Using a mouse model of type 1 diabetes and experimental myocardial infarction, preliminary data suggest diabetes and myocardial infarction synergize to accelerated myeloid cell death resulting in acceleration of the underlying disease – atherosclerosis.
Jenny Kanter, PhD
UW Medicine Diabetes Institute
750 Republican Street, Box 358062
Seattle, WA 98109
Jenny Kanter: (206) 616-6095
Fax: (206) 543-3567
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