Professor, Internal Medicine
The major focus of the laboratory is to determine the impact of various genetic alterations on atherosclerosis and arterial thrombosis using in vivo mouse models. We have developed models of vascular injury in the setting of atherosclerosis that allow us to identify the impact of many genes and conditions on atherothrombosis. We have recently used these mouse models to study links between obesity, diabetes and vascular endpoints. We have demonstrated that factors produced by adipocytes are capable of directly affecting atherosclerosis and arterial thrombosis. In addition, while surveying factors in the plasma that are increased in vascular inflammatory conditions, including diabetes and atherosclerosis, we have identified factors that are consistently and markedly elevated. Importantly, we have now shown that these factors serve as highly informative biomarkers since they represent specific interactions between leukocytes and endothelial cells. Additional experiments designed to determine their role in vascular and adipose inflammation are underway. To address the broader role of adipose tissue inflammation in vascular disease, we have recently developed a model of visceral fat inflammation and demonstrated that visceral, but not subcutaneous fat inflammation, is sufficient to accelerate atherosclerosis – in the absence of diabetes. Efforts are ongoing to identify the specific proatherogenic factors that are released from inflammatory visceral fat.