Biomechanical modulation of endothelial phenotype: implications for health and disease.
The functional phenotypic plasticity of the vascular endothelium relies on the ability of individual endothelial cells to integrate and transduce both humoral and biomechanical stimuli from their surrounding environments. Increasing evidence strongly suggests that biomechanical stimulation is a critical determinant of endothelial gene expression and the functional phenotypes displayed by these cells in several pathophysiological conditions. Herein we discuss the types of biomechanical forces that endothelial cells are constantly exposed to within the vasculature, explain how these biomechanical stimuli serve as regulators of endothelial function and discuss the increasing evidence that "atherosclerosis-protective" or "atherosclerosis-prone" haemodynamic environments can be important causative factors for atherogenesis via the differential regulation of endothelial transcriptional programmes.
García-Cardeña
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Center for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, 77 Avenue Louis Pasteur, NRB-7, 02115 MA, Boston, USA.
Gimbrone
M A
MA
D000818:Animals; D050197:Atherosclerosis / Q000188:drug therapy / Q000235:genetics / Q000503:physiopathology*; D001696:Biomechanical Phenomena; D001775:Blood Circulation; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D005786:Gene Expression Regulation; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D051741:Kruppel-Like Transcription Factors / Q000235:genetics / Q000378:metabolism; D010641:Phenotype; D013314:Stress, Mechanical
D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; C096161:KLF2 protein, human; D051741:Kruppel-Like Transcription Factors