Key result
Genetic quantitative and qualitative abnormalities of platelet membrane glycoprotein VI (GPVI) are rarely reported in humans but play a major role in thrombosis.
Why the study?
Platelet membrane GPVI plays a major role in thrombosis without being essential for physiological hemostasis, but human genetic GPVI deficiencies are rarely reported.
This review summarizes current knowledge on rare genetic quantitative and qualitative defects of platelet glycoprotein VI, a key receptor in thrombus formation.
Answers are grounded in this paper and cite their sources.
GPVI defects warrant consideration in select thrombotic cases; leaves open targeted antiplatelet strategies pending prospective data.
Platelet membrane glycoprotein VI (GPVI) is increasingly recognized as an important receptor for thrombus formation and growth. Numerous arguments have been published indicating that GPVI plays a major role in thrombosis without being essential for physiological hemostasis. In humans, GPVI deficiencies are rarely reported. These are most often deficiencies occurring in the context of autoimmunity and, more rarely, genetic deficits. The purpose of this review is to compile data on the quantitative and qualitative genetic abnormalities of GPVI.
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Jandrot‐Perrus et al. (2019) conducted a review in Platelet glycoprotein VI genetic defects. Platelet glycoprotein VI genetic defects was evaluated. Genetic quantitative and qualitative abnormalities of platelet membrane glycoprotein VI (GPVI) are rarely reported in humans but play a major role in thrombosis.
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