Abstract
Antiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by thromboembolism, obstetric complications, and the presence of antiphospholipid antibodies (aPL). Extracellular vesicles (EVs) play a key role in intercellular communication and connectivity and are known to be involved in endothelial and vascular pathologies. Despite well-characterized in vitro and in vivo models of APS pathology, the field of EVs remains largely unexplored. This review recapitulates recent findings on the role of EVs in APS, focusing on their contribution to endothelial dysfunction. Several studies have found that APS patients with a history of thrombotic events have increased levels of EVs, particularly of endothelial origin. In obstetric APS, research on plasma levels of EVs is limited, but it appears that levels of EVs are increased. In general, there is evidence that EVs activate endothelial cells, exhibit proinflammatory and procoagulant effects, interact directly with cell receptors, and transfer biological material. Future studies on EVs in APS may provide new insights into APS pathology and reveal their potential as biomarkers to identify patients at increased risk.
Highlights
Antiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by thrombosis and/or obstetric complications with persistent presence of antiphospholipid antibodies [1]. aPL are a heterogeneous group of autoantibodies, of which anti-cardiolipin, anti-β2 glycoprotein I, and lupus anticoagulant (LA) are included in the laboratory criteria for the diagnosis of APS [2]
Medium/large platelet Extracellular vesicles (EVs) isolated from pregnant APS patients with a history of recurrent miscarriage increased the levels of intracellular adhesion molecule-1 (ICAM-1), VCAM-1, and TNFα and increased adhesion of monocytes to endothelial cells compared to stimulation with EVs derived from healthy pregnant women
Endothelial dysfunction is a hallmark of vascular disorders, and EVs have been found to play an important role in hemostasis
Summary
Antiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by thrombosis and/or obstetric complications with persistent presence of antiphospholipid antibodies (aPL) [1]. aPL are a heterogeneous group of autoantibodies, of which anti-cardiolipin (anti-aCL), anti-β2 glycoprotein I (anti-β2GPI), and lupus anticoagulant (LA) are included in the laboratory criteria for the diagnosis of APS [2]. The most common classification of EVs used in the literature is the division of different EVs into subtypes, such as endosomal-derived exosomes (nanovesicles), membrane-derived microvesicles (microparticles or ectosomes), and apoptotic bodies. This classification is based on the assignment of a specific EV to a particular biogenesis pathway, which remains very difficult to assess [6]. In contrast to previous reviews [14,15,16], this review separately describes and examines the characteristics of EVs isolated from plasma of both thrombotic and obstetric APS patients, as well as includes studies examining the in vitro effects of aPL on EV release
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