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

Autor:	Liebeskind DS; Department of Neurology, Neurovascular Imaging Research Core and UCLA Stroke Center, University of California, Los Angeles, Los Angeles, CA, United States., Hinman JD; Department of Neurology, Neurovascular Imaging Research Core and UCLA Stroke Center, University of California, Los Angeles, Los Angeles, CA, United States., Kaneko N; Department of Neurology, Neurovascular Imaging Research Core and UCLA Stroke Center, University of California, Los Angeles, Los Angeles, CA, United States., Kitajima H; Department of Neurology, Neurovascular Imaging Research Core and UCLA Stroke Center, University of California, Los Angeles, Los Angeles, CA, United States., Honda T; Department of Neurology, Neurovascular Imaging Research Core and UCLA Stroke Center, University of California, Los Angeles, Los Angeles, CA, United States., De Havenon AH; Department of Neurology, University of Utah, Salt Lake City, UT, United States., Feldmann E; Department of Neurology, The University of Massachusetts Medical School-Baystate, Springfield, MA, United States., Nogueira RG; Department of Neurology, Marcus Stroke & Neuroscience Center, Emory University School of Medicine, Atlanta, GA, United States., Prabhakaran S; Department of Neurology, The University of Chicago, Chicago, IL, United States., Romano JG; Department of Neurology, University of Miami, Miami, FL, United States., Callas PW; Department of Biostatistics, University of Vermont, Burlington, VT, United States., Schneider DJ; Department of Medicine, Cardiovascular Research Institute, University of Vermont, Burlington, VT, United States.
Jazyk:	angličtina
Zdroj:	Frontiers in neurology [Front Neurol] 2021 Feb 25; Vol. 12, pp. 646309. Date of Electronic Publication: 2021 Feb 25 (Print Publication: 2021).
DOI:	10.3389/fneur.2021.646309
Abstrakt:	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. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2021 Liebeskind, Hinman, Kaneko, Kitajima, Honda, De Havenon, Feldmann, Nogueira, Prabhakaran, Romano, Callas and Schneider.)
Databáze:	MEDLINE
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