AI Article Synopsis
- The formation of atherosclerotic lesions is linked to disturbed blood flow in specific arterial geometries, indicating that hemodynamic forces significantly contribute to atherosclerosis development.
- The vascular endothelium can differentiate between various blood flow forces and convert these mechanical signals into genetic programs that impact its function.
- The review also examines how certain blood flow conditions act as local risk factors for atherosclerosis and discusses the potential for activating protective genes to improve vascular health.
Article 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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4564111 | PMC |
| http://dx.doi.org/10.1016/j.carpath.2012.06.006 | DOI Listing |
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