Cardeza Foundation for Hematologic Research, Thomas Jefferson University, Philadelphia, PA; and.
Department of Emergency Medicine, School of Medicine, University of Maryland, Baltimore, MD.
Blood Adv. 2021 Mar 9;5(5):1576-1584. doi: 10.1182/bloodadvances.2020002888.
Ischemic stroke is a leading cause of morbidity and mortality worldwide and, despite reperfusion either via thrombolysis or thrombectomy, stroke patients often suffer from lifelong disabilities. These persistent neurological deficits may be improved by treating the ischemia/reperfusion (I/R) injury that occurs following ischemic stroke. There are currently no approved therapies to treat I/R injury, and thus it is imperative to find new targets to decrease the burden of ischemic stroke and related diseases. Platelets, cell fragments from megakaryocytes, are primarily known for their role in hemostasis. More recently, investigators have studied the nonhemostatic role of platelets in inflammatory pathologies, such as I/R injury after ischemic stroke. In this review, we seek to provide an overview of how I/R can lead to platelet activation and how activated platelets, in turn, can exacerbate I/R injury after stroke. We will also discuss potential mechanisms by which platelets may ameliorate I/R injury.
缺血性中风是全球发病率和死亡率的主要原因，尽管通过溶栓或血栓切除术进行再灌注，但中风患者经常遭受终身残疾。通过治疗缺血性中风后发生的缺血/再灌注 (I/R) 损伤，可以改善这些持续存在的神经功能缺损。目前尚无批准的治疗 I/R 损伤的疗法，因此必须寻找新的靶点来减轻缺血性中风和相关疾病的负担。血小板是巨核细胞的细胞碎片，主要因其在止血中的作用而闻名。最近，研究人员研究了血小板在炎症性病理中的非止血作用，例如缺血性中风后的 I/R 损伤。在这篇综述中，我们旨在概述 I/R 如何导致血小板激活，以及激活的血小板如何反过来加重中风后的 I/R 损伤。我们还将讨论血小板可能减轻 I/R 损伤的潜在机制。
