ArticleThrombosis journal2016
Posttranslational forms of beta 2-glycoprotein I in the pathogenesis of the antiphospholipid syndrome.
Article in Thrombosis journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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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.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Bridging the gap between CVD and COVID-19: the oxidized LDL hypothesis.Frontiers in medicine · 2025Article
- Antibody profiles in the mosaic of 'seronegative' APS syndrome.Clinical and experimental immunology · 2024Article
- Managing Antiphospholipid Syndrome in Children and Adolescents: Current and Future Prospects.Paediatric drugs · 2022Review
- Endothelial dysfunction and COVID-19 (Review).Biomedical reports · 2021Review
- Specific domain V reduction of beta-2-glycoprotein I induces protein flexibility and alters pathogenic antibody binding.Scientific reports · 2021Article
- Interactions between Beta-2-Glycoprotein-1 and Phospholipid Bilayer-A Molecular Dynamic Study.Membranes · 2020Article
- COVID-19 as a Blood Clotting Disorder Masquerading as a Respiratory Illness: A Cerebrovascular Perspective and Therapeutic Implications for Stroke Thrombectomy.Journal of neuroimaging : official journal of the American Society of Neuroimaging · 2020Review
- Article
- The role of beta-2-glycoprotein I in health and disease associating structure with function: More than just APS.Blood reviews · 2020Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The antiphospholipid syndrome (APS) is an autoimmune disease characterised by a procoagulant state that predisposes to recurrent thrombosis and miscarriages. Two major discoveries have advanced our understanding of the underlying complex pathogenesis of the APS. The first was the discovery that beta-2 glycoprotein-1 (β2GPI) is the major auto antigen in APS. The second was the discovery in more recent years that β2GPI contains allosteric disulphide bonds susceptible to posttranslational modification that may be involved in the development of autoantibodies in APS. The main allosteric disulphide bond in the fifth domain of β2GPI can exist in two redox states: free thiol or oxidised. It is the conformational transformation of β2GPI from its free thiol form to its more immunogenic oxidised form that exposes neo-epitopes on the first and fifth domains. The purpose of this review is to highlight the recent findings on the posttranslational forms of β2GPI in the pathogenesis of APS. We suggest that novel assays quantitating the different redox forms of β2GPI in plasma or serum may be used to supplement existing clinical and laboratory assays to more accurately stratify risk of thrombosis or miscarriage in APS patients.
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Registered trials
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.