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Cardiovasc Pathol. 2013 Jan-Feb;22(1):9-15. doi: 10.1016/j.carpath.2012.06.006. Epub 2012 Jul 18.

Vascular endothelium, hemodynamics, and the pathobiology of atherosclerosis.

Author information

1
Center for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. mgimbrone@rics.bwh.harvard.edu

Abstract

The localization of atherosclerotic lesion formation to regions of disturbed blood flow associated with certain arterial geometries, in humans and experimental animals, suggests an important role for hemodynamic forces in the pathobiology of atherosclerosis. There is increasing evidence that the vascular endothelium, which is directly exposed to various fluid mechanical forces generated by pulsatile blood flow, can discriminate among these different biomechanical stimuli and transduce them into genetic regulatory programs that modulate endothelial function. In this brief review, we discuss how biomechanical stimuli generated by blood flow can influence endothelial functional phenotypes, and explore the working hypothesis of "atheroprone" hemodynamic environments as "local risk factors" in atherogenesis. In addition, we consider the therapeutic implications of the activation of "atheroprotective genes" and their role as "critical regulatory nodes" in vascular homeostasis.

PMID:
22818581
PMCID:
PMC4564111
DOI:
10.1016/j.carpath.2012.06.006
[Indexed for MEDLINE]
Free PMC Article

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