Atherosclerosis, the process that culminates in a heart attack, is the focus of this discipline. The conventional view that high grade occlusive, stenotic coronary lesions represent the final step in a continuum that begins with fatty streaks and culminates in high grade stenosis resulting in acute coronary syndromes has been modified because thrombotic occlusion is frequently the result of rupture of non-critically stenotic plaques.
Disruption of 'vulnerable' plaques and subsequent thrombosis can lead to intermittent, sudden plaque growth and precipitate acute coronary syndromes.
Features of atherosclerotic plaques that predispose to rupture include a necrotic lipid core occupying more than 40% of plaque volume, a thin fibrous cap, decreased numbers of vascular smooth muscle cells, and accumulation of macrophages at the edge or so-called shoulder of the plaque.
The primary goal of our vascular biology group is to define mechanisms responsible for the development of vulnerable atherosclerotic plaques to provide therapeutic targets for prevention or retardation of their evolution and diminution of rupture.
A robust program that employs transgenic mice with atherosclerosis is complemented by comprehensive quantitative assessment of the composition of atherosclerotic plaques.
The role of diabetes and insulin resistance in accelerating progression of atherosclerosis is a particular interest, as are intracellular signaling mechanisms responsible for changes in vascular smooth muscle cell phenotype.
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