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For many years, vascular biologists and pathologists have known that atherosclerosis is a spatially discontinuous disease; plaque tends to form in specific locations, especially branch points in large arteries, where blood flow is discontinuous and disordered. Furthermore, plaque formation progresses temporally from the proximal arterial tree to more distal vessels. It is also well known that vascular endothelial cells are sensitive to shear stress patterns and blood flow1 and, in fact, express a robust mechanosensory system made up of intracellular signaling pathways that are triggered by integrins, selectins, and cilia.2 Unidirectional flow in straight vessels, such as the distal aorta, is atheroprotective, whereas disordered flow (DF) at curvatures and branch points, such as the aortic arch, promotes inflammatory signaling, endothelial dysfunction, leukocyte recruitment, and plaque formation.3 An article by Le Master et al4 published in this issue of Arteriosclerosis, Thrombosis, and Vascular Biology presents elegant new data that helps integrate these observations into a pathogenic model that relates disordered blood flow to upregulated endothelial cell expression of the scavenger receptor CD36 (cluster of differentiation 36), increased uptake of oxidized lipids, and increased endothelial cell stiffness.See accompanying article on page 64 The …

arteriosclerosis, thrombosis, and vascular biology

Oxidized Lipid Uptake by Scavenger Receptor CD36 (Cluster of Differentiation 36) Modulates Endothelial Surface Properties and May Contribute to Atherogenesis