Department of Internal Medicine and Medical Specialties, Sapienza University of Rome, Rome, Italy.
Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
J Thromb Haemost. 2018 Feb;16(2):220-230. doi: 10.1111/jth.13910. Epub 2017 Dec 26.
Platelets are small anucleated cells that constantly patrol the cardiovascular system to preserve its integrity and prevent excessive blood loss where the vessel lining is breached. Their key challenge is to form a hemostatic plug under conditions of high shear forces. To do so, platelets have evolved a molecular machinery that enables them to sense trace amounts of signals at the site of damage and to rapidly shift from a non-adhesive to a pro-adhesive state. However, this highly efficient molecular machinery can also lead to unintended platelet activation and cause clinical complications such as thrombocytopenia and thrombosis. Thus, several checkpoints are in place to tightly control platelet activation and adhesiveness in space and time. In this review, we will discuss select negative regulators of platelet activation, which are critical to maintain patrolling platelets in a quiescent, non-adhesive state and/or to limit platelet adhesion to sites of injury.
血小板是一种无核的小细胞，它们不断在心血管系统中巡逻，以保持其完整性并防止血管内层破裂导致过度失血。它们的主要挑战是在高剪切力下形成止血塞。为此，血小板进化出了一种分子机制，使它们能够在损伤部位感知微量信号，并迅速从非黏附状态转变为促黏附状态。然而，这种高效的分子机制也可能导致血小板的意外激活，并引发临床并发症，如血小板减少症和血栓形成。因此，有几个检查点可以在空间和时间上严格控制血小板的激活和黏附。在这篇综述中，我们将讨论血小板激活的一些负调控因子，这些因子对于维持静息、非黏附状态的巡逻血小板以及/或限制血小板黏附到损伤部位至关重要。
