VWF, Platelets and the Antiphospholipid Syndrome

Shengshi Huang, Marisa Ninivaggi, Walid Chayoua, Bas de Laat*

*Corresponding author for this work

Research output: Contribution to journal(Systematic) Review article peer-review


The antiphospholipid syndrome (APS) is characterized by thrombosis and/or pregnancy morbidity with the persistent presence of antiphospholipid antibodies (aPLs). Laboratory criteria for the classification of APS include the detection of lupus anticoagulant (LAC), anti-cardiolipin (aCL) antibodies and anti-beta 2glycoprotein I (a beta 2GPI) antibodies. Clinical criteria for the classification of thrombotic APS include venous and arterial thrombosis, along with microvascular thrombosis. Several aPLs, including LAC, a beta 2GPI and anti-phosphatidylserine/prothrombin antibodies (aPS/PT) have been associated with arterial thrombosis. The Von Willebrand Factor (VWF) plays an important role in arterial thrombosis by mediating platelet adhesion and aggregation. Studies have shown that aPLs antibodies present in APS patients are able to increase the risk of arterial thrombosis by upregulating the plasma levels of active VWF and by promoting platelet activation. Inflammatory reactions induced by APS may also provide a suitable condition for arterial thrombosis, mostly ischemic stroke and myocardial infarction. The presence of other cardiovascular risk factors can enhance the effect of aPLs and increase the risk for thrombosis even more. These factors should therefore be taken into account when investigating APS-related arterial thrombosis. Nevertheless, the exact mechanism by which aPLs can cause thrombosis remains to be elucidated.

Original languageEnglish
Article number4200
Number of pages14
JournalInternational journal of molecular sciences
Issue number8
Publication statusPublished - Apr 2021


  • antiphospholipid syndrome
  • arterial thrombosis
  • von Willebrand factor
  • platelet
  • antiphospholipid antibody

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