- Harvard Medical School
My laboratory has investigated the molecular and cellular mechanisms of atherosclerosis. We have advanced the hypothesis that inflammation drives all phases of atherogenesis and its complications in vitro, in analyses of human disease tissue, in experimental animals, and ultimately in human populations and clinical trials. We have systematically evaluated the roles of inflammatory mediators in vascular biology, atheroma initiation, progression, and complications. We have also focused the pathogenesis of transplantation-associated arteriopathy, the regulation of the expression and activity of these matrix-degrading proteinases in relation to mechanisms of plaque disruption, and the use of inflammatory biomarkers as a translational tool. We have worked with our colleague Dr. Benjamin Ebert on defining a newly recognized, common, and potent cardiovascular risk factor, clonal hematopoiesis, and have identified inflammatory mechanisms that likely account for part of the aggravation of cardiovascular outcomes that does not depend on traditional risk factors.
I have trained generations of fellows and residents, many of whom now occupy leadership positions worldwide. I instigated and helped to lead the first large scale randomized clinical trial that established inflammation as a therapeutic target in cardiovascular disease, the Canakinumab Anti-Inflammatory Thrombosis Outcomes Study (CANTOS).
|Sep. 11 (Fri)
||Room 1 & 2 & 3
||Plenary Lecture 10
Clonal Hematopoiesis at the Crossroads of Aging, Cancer, and Cardiovascular Disease
||Clonal Hematopoiesis at the Crossroads of Aging, Cancer, and Cardiovascular Disease
|Sep. 12 (Sat)
||An Update on Anti-Inflammatory Therapy for Atherosclerosis: CANTOS and Beyond.