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Updated: Jul 14, 2026

Ferric Chloride-induced Murine Thrombosis Models
Published on: September 5, 2016
Mechanisms of aPL-mediated thrombosis: effects of aPL on endothelium and platelets
Mariano E Vega-Ostertag1, Silvia S Pierangeli
1Laboratory of Hemostasia and Thrombosis, Instituto Fares Taie, Rivadavia, Mar del Plata, Buenos Aires, Argentina. hemostasia@farestaie.com.ar
Antiphospholipid antibodies (aPL) are associated with thrombosis and pregnancy loss in patients with systemic lupus erythematosus and antiphospholipid syndrome. Strong evidence demonstrates that aPL are pathogenic in vivo from studies that utilized animal models of thrombosis, endothelial cell activation, and pregnancy loss. However, the mechanisms by which aPL mediate disease are only partially understood, and our knowledge is limited by the polyspecificity of the antibodies, the multiple potential end-organ targets, and the variability of the clinical context in which the disease may present. This review discusses and summarizes the most current data available on molecular interactions and pathogenic mechanisms in antiphospholipid syndrome.
Antiphospholipid antibodies (aPL) are associated with thrombosis and pregnancy loss in patients with systemic lupus erythematosus and antiphospholipid syndrome. Strong evidence demonstrates that aPL are pathogenic in vivo from studies that utilized animal models of thrombosis, endothelial cell activation, and pregnancy loss. However, the mechanisms by which aPL mediate disease are only partially understood, and our knowledge is limited by the polyspecificity of the antibodies, the multiple potential end-organ targets, and the variability of the clinical context in which the disease may present. This review discusses and summarizes the most current data available on molecular interactions and pathogenic mechanisms in antiphospholipid syndrome.
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