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Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

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Proteins upregulated in thrombotic antiphospholipid syndrome linked to platelet function in contrast with

Silvia Mancuso¹, Claudia Ciancarella², Luca Rapino¹

¹Department of Medical and Cardiovascular Sciences, University of Rome La Sapienza, Rome, Italy.

Lupus Science & Medicine

|November 7, 2025

Abstract

Background:

Antiphospholipid 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.

Objective:

The 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.

Methods:

We 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.

Results:

Of 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.

Conclusion:

Our 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.

Keywords:

Antibodies Antibodies, Anticardiolipin Antiphospholipid Syndrome Autoimmune Diseases Lupus Erythematosus, Systemic

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Keywords:

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