Pathogenesis of antiphospholipid syndrome and recommended areas for research: “first hit” circulating antiphospholipid antibodies (aPLs) and underlying endothelial dysfunction and “second hit” inflammatory insult result in impaired nitric oxide (NO)–dependent endothelial function, accelerated atherosclerosis, nonatherosclerotic vasculopathy, platelet activation and aggregation, and complement system activation. Research in aPL and beta-2 glycoprotein 1 receptor (β2-GP1) interaction, β2-GP1 and apolipoprotein E receptor 2 (apoER2) interaction, and complement system activation is recommended. | C5a = complement component 5a fragment; C5b = complement component 5b fragment. | Corban, M. T., Duarte-Garcia, A., McBane, R. D., Matteson, E. L., Lerman, L. O., & Lerman, A. (2017). Antiphospholipid Syndrome. Journal of the American College of Cardiology, 69(18), 2317 LP – 2330. https://doi.org/10.1016/j.jacc.2017.02.058

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