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The role of platelets in antiphospholipid syndrome
- Source :
- Platelets, Vol 28, Iss 8, Pp 762-766 (2017)
- Publication Year :
- 2017
- Publisher :
- Taylor & Francis Group, 2017.
-
Abstract
- Despite extensive research, the pathogenesis of antiphospholipid syndrome (APS) remains obscure in many aspects. However, it is widely accepted that thrombosis is the result of a hypercoagulable state caused by antibodies directed against β2-glycoprotein I (β2-GPI), a protein whose physiological role is unknown. Although underestimated, platelets may be involved in APS and its thrombotic manifestations, especially arterial, in several ways. Thrombocytopenia is the most relevant non-criteria manifestation of APS, possibly caused by direct binding of anti-β2-GPI antibodies or anti-β2-GPI–β2-GPI complexes. On the other hand, platelets may have a key role in APS-related thrombosis due to the presence of multiple receptors that can interact with anti-β2-GPI antibodies (especially apolipoprotein E receptor 2’ (apoER2’) and glycoprotein Ibα (GPIbα)) with consequent release of different procoagulant mediators such as thromboxane B2, platelet factor 4 (PF4), and platelet factor 4 variant (CXCL4L1). The aim of this review is to put together evidence on the possible role of platelets in APS and to stimulate further research on the issue.
Details
- Language :
- English
- ISSN :
- 09537104 and 13691635
- Volume :
- 28
- Issue :
- 8
- Database :
- Directory of Open Access Journals
- Journal :
- Platelets
- Publication Type :
- Academic Journal
- Accession number :
- edsdoj.6d56ce052ae4459b34bb03ada0cc83d
- Document Type :
- article
- Full Text :
- https://doi.org/10.1080/09537104.2017.1280150