Evidence map›Paper›PMID 40181965›Full record

ReviewFrontiers in immunology2025

Mechanism of antiphospholipid antibody-mediated thrombosis in antiphospholipid syndrome.

Leiyi Yang, Ruibing Guo, Hongjiang Liu, Bo Chen, Changpei Li, Ruiting Liu, Shuyi Liao, Qibing Xie, Geng Yin

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed.

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  18. Quantifying Lupus Anticoagulant Interference in Intrinsic Coagulation Factor Activity Assays and Evaluating the Corrective Performance of the SCT-Based Method.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Leiyi Yang *Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, China.
Ruibing Guo *Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, China.
Hongjiang Liu *Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, China.
Bo ChenDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, China.
Changpei LiDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, China.
Ruiting LiuDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, China.
Shuyi LiaoDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, China.
Qibing XieDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, China.
Geng YinHealth Management Center, General Practice Medical Center, West China Hospital, Sichuan University, Chengdu, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antiphospholipid syndrome (APS) is an autoimmune disease characterized by the occurrence of thrombotic or obstetrical events in patients with persistent antiphospholipid antibodies (aPL). Thrombotic events, the primary pathological hallmarks and clinical manifestations, are among the leading causes of mortality in APS. Our understanding of the mechanism underlying APS-related thrombosis has significantly advanced in recent years. The presence of aPL, particularly anti-β2-glycoprotein I (anti-β2GPI) antibodies, is a major driver of thrombosis. The proposed pathophysiological mechanisms of aPL-mediated pro-thrombotic events can be broadly categorized into three types: disruption of anticoagulant reactions and fibrinolysis, interference with coagulation cascade cells, and complement activation. A triggering 'second hit' is typically necessary to initiate thrombosis. The development of animal models of APS has further refined our understanding of the role of aPL in thrombosis. In this review, we focused on the role of β2GPI-dependent aPL in thrombosis of thrombotic APS.

Indexed as

Antibodies, AntiphospholipidAntiphospholipid SyndromeThrombosisAnimalsbeta 2-Glycoprotein IBlood CoagulationComplement ActivationHumansAntibodies, Antiphospholipidbeta 2-Glycoprotein Iantiphospholipid antibodyantiphospholipid syndromethrombotic eventtwo hit modelβ2-glycoprotein I

Identifiers

PMID40181965
PMCPMC11966034

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.