Taylor K A, Pugh N
Department of Biomedical and Forensic Sciences, Faculty of Science and Technology, Anglia Ruskin University, Cambridge, CB1 1PT, UK.
Metallomics. 2016 Feb;8(2):144-55. doi: 10.1039/c5mt00251f.
Platelets are the primary cellular determinants of haemostasis and pathological thrombus formation leading to myocardial infarction and stroke. Following vascular injury or atherosclerotic plaque rupture, platelets are recruited to sites of damage and undergo activation induced by a variety of soluble and/or insoluble agonists. Platelet activation is a multi-step process culminating in the formation of thrombi, which contribute to the haemostatic process. Zinc (Zn(2+)) is acknowledged as an important signalling molecule in a diverse range of cellular systems, however there is limited understanding of the influence of Zn(2+) on platelet behaviour during thrombus formation. This review evaluates the contributions of exogenous and intracellular Zn(2+) to platelet function and assesses the potential pathophysiological implications of Zn(2+) signalling. We also provide a speculative assessment of the mechanisms by which platelets could respond to changes in extracellular and intracellular Zn(2+) concentration.
血小板是止血和导致心肌梗死及中风的病理性血栓形成的主要细胞决定因素。血管损伤或动脉粥样硬化斑块破裂后，血小板被募集到损伤部位，并受到多种可溶性和/或不溶性激动剂诱导而活化。血小板活化是一个多步骤过程，最终形成血栓，这有助于止血过程。锌（Zn(2+)）在多种细胞系统中被认为是一种重要的信号分子，然而，对于Zn(2+)在血栓形成过程中对血小板行为的影响了解有限。本综述评估了外源性和细胞内Zn(2+)对血小板功能的作用，并评估了Zn(2+)信号传导的潜在病理生理意义。我们还对血小板可能对细胞外和细胞内Zn(2+)浓度变化作出反应的机制进行了推测性评估。
