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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:2101.)
© 2008 American Heart Association, Inc.

Brief Reviews

The Role of Cellular Adaptation to Mechanical Forces in Atherosclerosis

Cornelia Hahn; Martin A. Schwartz

From the Department of Microbiology (C.H., M.A.S.), University of Virginia, and the Robert M. Berne Cardiovascular Research Center, Mellon Prostate Cancer Research Center and Departments of Cell Biology and Biomedical Engineering (M.A.S.), University of Virginia, Charlottesville.

Correspondence to Martin Schwartz, Robert M. Berne Cardiovascular Research Center, Mellon Prostate Cancer Research Center and Departments of Cell Biology and Biomedical Engineering, University of Virginia, Charlottesville, VA 22908. E-mail maschwartz{at}virginia.edu

Atherosclerosis is a chronic inflammatory disease that originates at regions of arteries exposed to disturbances in fluid flow and results in progressive plaque formation in those areas. Recent work on cellular responses to flow has identified potential mechanosensors and pathways that may influence disease progression. These results led us to hypothesize that the same mechanisms that mediate adaptive responses in the vasculature become maladaptive at sites of disturbed flow. Subsequent changes in gene expression and matrix remodeling help to entrain these inflammatory pathways. These events synergize with systemic risk factors such as hyperlipidemia, smoking, and diabetes, leading to disease progression.

Key Words: fluid shear stress • endothelial • smooth muscle • inflammation • disturbed flow • laminar flow

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