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- W2900040420 abstract "Introduction: Even though our understanding of the antiphospholipid syndrome (APS) has improved tremendously over the last decades, we are still not in a position to replace symptomatic anticoagulation by pathogenesis based causal treatments.Areas covered: Recent years have provided further insights into pathogenetically relevant mechanisms. These include a differentiation of pathogenic subtypes of antiphospholipid antibodies (aPL), novel mechanisms modulating disease activity, for example, extracellular vesicles and microRNA, and novel players in pathogenesis, for example, neutrophils and neutrophil extracellular traps (NETs).Expert commentary: It is evident that aPL induce a proinflammatory and procoagulant state and recent data suggest that different aPL species activate different signaling pathways which sometimes converge into a common cellular response. This implies that presence of more than one aPL species may disproportionally increase the risk for the major manifestations of APS, that is, thrombosis and fetal loss. Further delineation of the pathogenic mechanisms will hopefully provide clues to causal rather than symptomatic treatments of APS." @default.
- W2900040420 created "2018-11-16" @default.
- W2900040420 creator A5066003145 @default.
- W2900040420 creator A5075174977 @default.
- W2900040420 date "2018-12-06" @default.
- W2900040420 modified "2023-09-27" @default.
- W2900040420 title "Pathogenesis of antiphospholipid syndrome: recent insights and emerging concepts" @default.
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- W2900040420 doi "https://doi.org/10.1080/1744666x.2019.1546578" @default.
- W2900040420 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30412684" @default.
- W2900040420 hasPublicationYear "2018" @default.
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