Clemetson K J, Clemetson J M
Theodor Kocher Institute, University of Berne, Switzerland.
Thromb Haemost. 2001 Jul;86(1):189-97.
Collagens are important platelet activators in the vascular subendothelium and vessel wall. Since the regulation of platelet activation is a key step in distinguishing normal haemostasis from pathological thrombosis, collagen interactions with platelets are important targets for pharmacological control. Platelets have two major receptors for collagens, the integrin alpha2beta1, with a major role in adhesion and platelet anchoring and the Ig superfamily member, GPVI, principally responsible for signalling and platelet activation. In addition, GPIb-V-IX, can be considered as an indirect collagen receptor acting via von Willebrand factor as bridging molecule and is essential for platelet interactions with collagen at high shear rates. There is some evidence for additional receptors, which may regulate the response to individual collagen types. This review discusses how these receptors work separately with specific agonists and proposes possible mechanisms for how they work together to regulate platelet activation by collagen, which remains controversial and poorly understood.
胶原蛋白是血管内皮下层和血管壁中重要的血小板激活剂。由于血小板激活的调节是区分正常止血与病理性血栓形成的关键步骤,胶原蛋白与血小板的相互作用是药理控制的重要靶点。血小板有两种主要的胶原蛋白受体,整合素α2β1,在黏附及血小板锚定中起主要作用,以及免疫球蛋白超家族成员糖蛋白VI(GPVI),主要负责信号传导和血小板激活。此外,糖蛋白Ib-V-IX可被视为一种间接的胶原蛋白受体,通过血管性血友病因子作为桥接分子发挥作用,对于高剪切速率下血小板与胶原蛋白的相互作用至关重要。有证据表明存在其他受体,它们可能调节对不同类型胶原蛋白的反应。本文综述讨论了这些受体如何分别与特定激动剂起作用,并提出了它们共同作用调节胶原蛋白介导的血小板激活的可能机制,这一过程仍存在争议且了解甚少。