SynthesisLupus science & medicine2025
Proteins upregulated in thrombotic antiphospholipid syndrome linked to platelet function in contrast with non-antiphospholipid-related thrombosis: insights from two systematic reviews.
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Abstract
backgroundAntiphospholipid syndrome (APS) is a systemic autoimmune disease characterised by thrombosis, pregnancy complications and other non-thrombotic manifestations in the presence of antiphospholipid antibodies (aPL). Since its identification in 1983, research on APS has progressed, but no targeted therapies other than anticoagulation are yet available, with a mortality rate of 9.3% after a 10-year follow-up.
objectiveThe aim of the current systematic literature reviews (SLRs) is to identify and compare upregulated proteins in patients with thrombotic APS (tAPS) and non-aPL thrombosis, thereby providing useful insights into APS pathogenesis.
methodsWe conducted two SLRs in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines to identify proteins upregulated in tAPS and non-aPL-related thrombosis. Eligible studies included observational controlled research and focused on proteomics. Gene Ontology (GO) enrichment and network analyses were performed on the identified proteins.
resultsOf 108 and 209 records identified, seven and 13 were included in the SLR for tAPS and non-aPL thrombosis, respectively. The review identified 118 upregulated proteins in tAPS and 319 in non-aPL-related thrombosis. GO analysis revealed distinct biological process enrichment: platelet aggregation, platelet activation and blood coagulation were predominant in tAPS, while haemostasis, coagulation and wound healing were central in non-aPL-related thrombosis. Molecular functions in tAPS centred on receptor and protein complex binding, while enzymatic activities dominated in non-aPL thrombosis.
conclusionOur findings highlight the central role of platelet-related processes in tAPS pathogenesis, distinguishing it from non-aPL thrombosis. By elucidating the unique proteomic and functional characteristics of tAPS, this study provides a foundation for future research into targeted therapies that address platelet involvement in APS pathogenesis.
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