A new animal model of atherosclerosis has allowed researchers to identify a host of genes turned on or off during the initial stages of the process, before a plaque appears in the affected blood vessel.
The results were published June 15 in Blood, the journal of the American Society of Hematology.
The model is the first to definitively show that disturbances in the patterns of blood flow in an artery determine where atherosclerosis will later appear, says senior author Hanjoong Jo, PhD, Ada Lee and Pete Correll professor in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University.
The first author of the paper is Chih-Wen Ni, a graduate student in biomedical engineering.
Atherosclerosis describes a process where the arterial walls thicken and harden, because of a gradual build-up of white blood cells, lipids and cholesterol. This process can lead to plaque formation, and eventually to heart attacks and strokes.
Jo says his team's results could provide insight into how aerobic exercise, known to provide protection against atherosclerosis, improves the patterns of blood flow and encourages protective genes to turn on in blood vessels.
Scientists have previously observed that atherosclerosis occurs preferentially in branched or curved regions of arteries, because of the "disturbed flow" branches and curves create. Constant, regular flow of blood appears to promote healthy blood vessels, while low or erratic flow can lead to disease.
The standard laboratory model of atherosclerosis has scientists feeding a high-fat diet to mice with mutations in a gene (ApoE) involved in removing fat and cholesterol from the blood. Even then, atherosclerosis usually takes a few months to develop. In these models, clogs in a mouse's arteries tend to appear in certain places, such as the aortic arch, but flow patterns are set up at birth and thus are poor gauges of caus
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