Bradford C. Berk: Picking Good Questions.

Abstract

As Brad Berk sees it, “All the work I do can pretty much fit under the heading of signal transduction in blood vessels.” This deceptively short phrase, however, covers decades of research into the cellular and genetic mechanisms that produce some of cardiovascular medicine’s most stubborn challenges: atherosclerosis, aneurysms, and pulmonary hypertension. Berk’s academic career has led him from the University of Rochester to Harvard Medical School, Emory University, and the University of Washington before circling back to Rochester. Currently, he holds the post of Distinguished University Professor in medicine, neurology, pathology, and pharmacology and physiology. He has founded and directed 2 multidepartment institutes: the Aab Cardiovascular Research Institute (CVRI; from 1999 to 2006) and the University of Rochester Neurorestoration Institute (URNI; from 2015 to the present). Bradford C. Berk While at the University of Washington, in 1998, he published with Oren Traub a review1 of what was then known about how changes in blood-flow profile (steady versus disturbed) influence vascular disease. Berk went on to develop a highly reproducible model2 for vascular remodeling of the carotid as mediated by blood-flow profile. The disturbed flow region shows the formation of intima—a pathological thickening of the vessel wall. Because this thickening is predictive for cardiovascular events, the identification of genetic factors that played a role in the process3 marked a significant advance in cardiovascular research. Together with Korshunov et al, Berk studied 3 disease processes that contribute to intima: endothelial dysfunction, inflammation, and smooth muscle growth. By performing a genetic linkage study to home in on regions of the mouse genome that contribute to the intima,4 Berk and Korshunov identified a specific gene ( RpL17 ) that accounts for smooth muscle cell growth. With Smolock et al,5,6 they found a key link to inflammation now identified …