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颅内动脉粥样硬化疾病中的内皮剪切应力与血小板FcγRIIa表达

Endothelial Shear Stress and Platelet FcγRIIa Expression in Intracranial Atherosclerotic Disease.

作者信息

Liebeskind David S, Hinman Jason D, Kaneko Naoki, Kitajima Hiroaki, Honda Tristan, De Havenon Adam H, Feldmann Edward, Nogueira Raul G, Prabhakaran Shyam, Romano Jose G, Callas Peter W, Schneider David J

机构信息

Department of Neurology, Neurovascular Imaging Research Core and UCLA Stroke Center, University of California, Los Angeles, Los Angeles, CA, United States.

Department of Neurology, University of Utah, Salt Lake City, UT, United States.

出版信息

Front Neurol. 2021 Feb 25;12:646309. doi: 10.3389/fneur.2021.646309. eCollection 2021.

Abstract

Intracranial atherosclerotic disease (ICAD) has been characterized by the degree of arterial stenosis and downstream hypoperfusion, yet microscopic derangements of endothelial shear stress at the luminal wall may be key determinants of plaque growth, vascular remodeling and thrombosis that culminate in recurrent stroke. Platelet interactions have similarly been a principal focus of treatment, however, the mechanistic basis of anti-platelet strategies is largely extrapolated rather than directly investigated in ICAD. Platelet FcγRIIa expression has been identified as a potent risk factor in cardiovascular disease, as elevated expression markedly increases the risk of recurrent events. Differential activation of the platelet FcγRIIa receptor may also explain the variable response of individual patients to anti-platelet medications. We review existing data on endothelial shear stress and potential interactions with the platelet FcγRIIa receptor that may alter the evolving impact of ICAD, based on local pathophysiology at the site of arterial stenosis. Current methods for quantification of endothelial shear stress and platelet activation are described, including tools that may be readily adapted to the clinical realm for further understanding of ICAD.

摘要

颅内动脉粥样硬化疾病(ICAD)的特征在于动脉狭窄程度和下游灌注不足,然而,管腔壁处内皮剪切应力的微观紊乱可能是斑块生长、血管重塑和血栓形成的关键决定因素,这些最终会导致复发性中风。血小板相互作用同样一直是治疗的主要焦点,然而,抗血小板策略的机制基础在很大程度上是外推而来的,而非在ICAD中直接进行研究。血小板FcγRIIa表达已被确定为心血管疾病的一个强大风险因素,因为表达升高会显著增加复发事件的风险。血小板FcγRIIa受体的差异激活也可能解释个体患者对抗血小板药物的不同反应。我们基于动脉狭窄部位的局部病理生理学,综述了关于内皮剪切应力以及与血小板FcγRIIa受体潜在相互作用的现有数据,这些相互作用可能会改变ICAD的进展影响。描述了目前用于量化内皮剪切应力和血小板激活的方法,包括可能容易应用于临床领域以进一步了解ICAD的工具。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0527/7947292/ab1cab5961c0/fneur-12-646309-g0001.jpg

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