血小板
中性粒细胞胞外陷阱
医学
血小板膜糖蛋白
P-选择素
冲程(发动机)
内皮
血小板活化
内科学
病理生理学
炎症
缺血
阿司匹林
药理学
氯吡格雷
免疫学
机械工程
工程类
作者
Frederik Denorme,John L. Rustad,Robert A. Campbell
出处
期刊:Current Opinion in Hematology
[Ovid Technologies (Wolters Kluwer)]
日期:2021-06-28
卷期号:28 (5): 301-307
被引量:24
标识
DOI:10.1097/moh.0000000000000665
摘要
In this review, we will describe how the combined ability of platelets and neutrophils to interact with each other drives ischemic stroke brain injury.Neutrophils are one of the first cells to respond during ischemic stroke. Although animals stroke models have indicated targeting neutrophils improves outcomes, clinical trials have failed to yield successful strategies. Platelets play a critical role in recruiting neutrophils to sites of injury by acting as a bridge to the injured endothelium. After initial platelet adhesion, neutrophils can rapidly bind platelets through P-selectin and glycoprotein Ibα. In addition, recent data implicated platelet phosphatidylserine as a novel key regulator of platelet-neutrophil interactions in the setting of ischemic stroke. Inhibition of procoagulant platelets decreases circulating platelet-neutrophil aggregates and thereby reduces infarct size. Platelet binding alters neutrophil function, which contributes to the injury associated with ischemic stroke. This includes inducing the release of neutrophil extracellular traps, which are neurotoxic and pro-thrombotic, leading to impaired stroke outcomes.Platelet-neutrophil interactions significantly contribute to the pathophysiology of ischemic stroke brain injury. Better understanding the mechanisms behind their formation and the downstream consequences of their interactions will lead to improved therapies for stroke patients.
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