title: Hemodynamic forces in endothelial dysfunction and vascular aging.
abstract: Aging is a key risk factor associated with the onset of cardiovascular disease. Notably, vascular aging and cardiovascular disease are both associated with endothelial dysfunction, or a marked decrease in production and bioavailability the vasodilator of nitric oxide (NO). As a result of decreased nitric oxide availability, aging vessels often exhibit endothelial cell senescence and increased oxidative stress. One of the most potent activators of NO production is fluid shear stress produced by blood flow. Interestingly, age-related decrease in NO production partially results from endothelial insensitivity to shear stress. While the endothelial cell response to fluid shear stress has been well characterized in recent years, the exact mechanisms of how the mechanical force of fluid shear stress is converted into intracellular biochemical signals are relatively unknown. Therefore, gaining a better knowledge of mechanosignaling events in endothelial cells may prove to be beneficial for developing potential therapies for cardiovascular diseases.
authors.affiliation: Department of Cell and Molecular Physiology, McAllister Heart Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
authors.forename: Caitlin
authors.initials: C
authors.lastname: Collins
authors.forename: Ellie
authors.initials: E
authors.lastname: Tzima
mesh_terms: D000375:Aging / Q000502:physiology*; D002318:Cardiovascular Diseases / Q000503:physiopathology* / Q000628:therapy; D042783:Endothelial Cells / Q000502:physiology; D004730:Endothelium, Vascular / Q000254:growth & development / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D040542:Mechanotransduction, Cellular; D013314:Stress, Mechanical