作者: Chris I. Jones , Natasha E. Barrett , Leonardo A. Moraes , Jonathan M. Gibbins , Denise E. Jackson
DOI: 10.1007/978-1-61779-307-3_23
关键词:
摘要: The response of platelets to changes in the immediate environment is always a balance between activatory and inhibitory signals, cumulative effect which either activation or quiescence. This true free flowing blood their regulation haemostasis thrombosis. In this review, we consider endogenous mechanisms that combine regulate platelet activation. These include those derived from endothelium (nitric oxide, prostacyclin, CD39), receptors on surface (platelet endothelial cell adhesion molecule-1, carcinoembryonic antigen molecule 1, G6b-B - including evidence for role Ig-ITIM superfamily members negative ITAM-associated GPVI platelet-collagen interactions GPCR-mediated signalling positive "outside-in" integrin α(IIb)β(3)-mediated signalling), intracellular (retinoic X receptor, glucocorticoid peroxisome proliferator-activated receptors, liver receptor), emerging pathways (canonical Wnt signalling, Semaphorin 3A, specific molecule, junctional molecule-A).