Molecular basis of the effects of shear stress on vascular endothelial cells.
By Yi-Shuan J. Li, J. Haga, Shu Chien. Journal of Biomechanics, 2005
916 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/90483e70df65b2cfea6ee947cd9c2cbe9225c676
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Citations in the corpus
- Effects of Disturbed Flow on Vascular Endothelium: Pathophysiological Basis and Clinical Perspectives (2011, background): “Vascular endothelial cells (ECs), which form the inner lining of blood vessel wall with direct exposure to blood flow, serve important homeostatic functions in response to various chemical and mechanical stimuli (87, 111, 125, 337, 485, 573).”
- Cell mechanics: integrating cell responses to mechanical stimuli. (2007, background): “Force imposed at specialized sites can be transmitted through the cytoskeleton to sites in the cell interior (155).”
- Endothelial Dysfunction and Hypertension. (2016, background): “ECs are exposed to the shear stress resulting from blood flow and can convert mechanical stimuli into intracellular or biochemical signals (e.g., proliferation, apoptosis, migration, permeability, remodeling and gene expression) (Li et al. 2005a).”
- Role of endothelial shear stress in the natural history of coronary atherosclerosis and vascular remodeling: molecular, cellular, and vascular behavior. (2007, background): “These pathways are activated simultaneously and ross-talk with each other; the great majority of them onverge into the mitogen-activated protein kinase MAPKs) cascade at various levels, suggesting the key role f MAPKs in ESS mechanotransduction (39).”
- Mechanotransduction in vascular physiology and atherogenesis (2009, background): “Interestingly, flow is a potent survival signal for ECs because it has effects on multiple signalling pathways, which include the phosphoinositide 3-kinase (PI3K), extracellular signal-regulated kinase 5 (ERK5; also known as mitogen-activated protein kinase 7 ( MAPK7 )) and NO pathway”
- Mechanotransduction and endothelial cell homeostasis: the wisdom of the cell. (2007, background): “, 12 dyn/cm(2)) to ECs causes Ras to become bound with GTP instead of GDP, and this is followed sequentially by the activation of MAPKs (29, 39, 67) and the MCP-1 expression (62).”