Many different forms of heart disease can be caused by atherosclerosis (hardening or furring of the arteries). Atherosclerosis is caused by the formation of plaques that bulge into the artery, narrowing the blood vessel.
One factor that determines how easily an atherosclerotic plaque forms is the shear stress that the blood flow puts on the walls of the blood vessels, with low shear stress (LSS) and oscillatory shear stress (OSS) being pro-atherogenic. But exactly how LSS and OSS mediate this pro-atherogenic effect has not be completely defined.
In a study appearing online on February 15 in advance of publication in the March print issue of the Journal of Clinical Investigation, Rob Krams and colleagues from the Erasmus Medical Center, The Netherlands, show that in mice, different types of shear stress induce the production of different soluble factors known as chemokines, and that the chemokine expression pattern influences the development of the atherosclerotic plaque.
LSS was shown to induce the production of more IP-10, GRO-alpha, and fractalkine than OSS, which in fact induced no fractalkine. This correlated with differences in the composition of the atherosclerotic plaques: LSS induced plaques with thinner fibrous caps and larger necrotic cores than OSS (characteristics associated with plaque rupture, which can cause heart attacks).
As blocking fractalkine function inhibited LSS-induced plaque growth and decreased plaque characteristics associated with plaque rupture, the authors suggest that targeting fractalkine might provide an effective therapy to prevent atherosclerotic plaque rupture and heart attacks.
Materials provided by Journal of Clinical Investigation. Note: Content may be edited for style and length.
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