PublisherAmerican Society of Hematology
MetadataShow full item record
AbstractIschemic 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. Copyright 2021 by The American Society of Hematology
SponsorsThis work was supported by National Institutes of Health, National Heart, Lung, and Blood Institute grant 2R01 HL113188-07 (U.P.N.), American Heart Association Grant-in-Aid Award #13GRNT16380023 (U.P.N.), an American Society of Hematology Bridge Grant (U.P.N.), and National Institutes of Health, National Institute of Neurological Disorders and Stroke grant R01 NS095205 (R.F.R.).
Identifier to cite or link to this itemhttp://hdl.handle.net/10713/15150
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