Epigenetics-mediated pathological alternations and their potential in antiphospholipid syndrome diagnosis and therapy

APS (antiphospholipid syndrome) is a systematic autoimmune disease accompanied with venous or arterial thrombosis and poor pregnant manifestations, partly attributing to the successive elevated aPL (antiphospholipid antibodies) and provoked prothrombotic and proinflammatory molecules production. Nowadays, most researches focus on the laboratory detection and clinic features of APS, but its precise etiology remains to be deeply explored. As we all know, the dysfunction of ECs (endothelial cells), monocytes, platelets, trophoblasts and neutrophils are key contributors to APS progression. Especially, their epigenetic variations, mainly including the promoter CpGs methylation, histone PTMs (post-translational modifications) and ncRNAs (noncoding RNAs), result in genes expression or silence engaged in inflammation initiation, thrombosis formation, autoimmune activation and APOs (adverse pregnancy outcomes) in APS. Given the potential of epigenetic markers serving as diagnostic biomarkers or therapeutic targets of APS, and the encouraging advancements in epigenetic drugs are being made. In this review, we would systematically introduce the epigenetic underlying mechanisms for APS progression, comprehensively elucidate the functional mechanisms of epigenetics in boosting ECs, monocytes, platelets, trophoblasts and neutrophils. Lastly, the application of epigenetic alterations for probing novel diagnostic, specific therapeutic and prognostic strategies would be proposed.