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A rare systemic autoimmune disease characterized by hypercoagulability with vascular thrombosis and, in women, pregnancy morbidity (miscarriages, severe pre-eclampsia, placental insufficiency) in the presence of serum antiphospholipid antibodies, such as lupus anticoagulant, anticardiolipin antibodies, and anti-beta2-glycoprotein 1 antibodies.
PCSK9 inhibitors enhance LDLR-mediated clearance of oxidized phospholipids while anti-C1q antibodies prevent classical complement pathway activation. This dual approach reduces both lipid-mediated endothelial dysfunction and complement-driven coagulation cascade activation in APS.
Resveratrol activates SIRT1 deacetylase, which suppresses PAD4 enzyme activity and histone H3 citrullination. This prevents neutrophil extracellular trap formation triggered by anti-β2-glycoprotein I antibodies, reducing the prothrombotic NET-platelet aggregates characteristic of APS.
Curcumin suppresses NF-κB p65 nuclear translocation and inhibits NLRP3 inflammasome activation, reducing IL-1β and IL-18 production. This dampens the inflammatory cascade that promotes β2-glycoprotein I conformational changes and reduces complement C5a-mediated thrombosis in APS patients.
Butyrate and propionate enhance FOXP3+ regulatory T cell function through HDAC inhibition and GPR43 signaling. Simultaneously, these SCFAs disrupt molecular mimicry between bacterial lipopolysaccharides and human phospholipids, reducing cross-reactive antiphospholipid antibody production.
Astragaloside IV from Astragalus membranaceus inhibits HMGB1 release and TLR4 signaling while promoting BECN1-mediated autophagy. This reduces NET formation by neutrophils and decreases anti-β2-glycoprotein I antibody-induced endothelial cell activation and tissue factor expression.
Bacosides from Brahmi cross the blood-brain barrier and upregulate BDNF expression through CREB phosphorylation. This enhances neuroplasticity and protects against anti-ribosomal P antibody-mediated neuronal damage in APS patients with cognitive dysfunction and mood disorders.
Senomorphic compounds selectively target p16INK4a-positive senescent endothelial cells that accumulate due to chronic antiphospholipid antibody exposure. This reduces SASP factor secretion (IL-6, VEGFA, PDGF) and restores endothelial nitric oxide synthase function, improving vascular homeostasis.