ArticleThe Journal of clinical investigation2008
Tracing the molecular pathogenesis of antiphospholipid syndrome.
Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- Molecular Mechanisms of Negative Effect of Systemic Lupus Erythematosus on Oogenesis and Meiotic Processes in Oocytes.International journal of molecular sciences · 2026Review
- Endometrial immune cell profile at the time of frozen embryo transfer as prognostic indicator of live birth.Frontiers in immunology · 2026Observational
- Article
- Oxidative stress in endothelial cells induced by the serum of women with different clinical manifestations of the antiphospholipid syndromeBiomedica : revista del Instituto Nacional de Salud · 2019Article
- Genome-wide DNA methylation analysis in primary antiphospholipid syndrome neutrophils.Clinical immunology (Orlando, Fla.) · 2018Article
- Clinical and laboratory characteristics of children positive for antiphospholipid antibodies.Blood transfusion = Trasfusione del sangue · 2012Article
- Neutrophil NETs in reproduction: from infertility to preeclampsia and the possibility of fetal loss.Frontiers in immunology · 2012Article
- Thrombophilia: 2009 update.Current treatment options in cardiovascular medicine · 2009Article
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Abstract
Fetal loss induced by antiphospholipid antibodies (aPLs) in mice is a complement-driven inflammatory condition. Engagement of the complement receptor C5aR on neutrophils induces expression of the principal initiator of the blood clotting mechanism, tissue factor (TF), and blocking this downstream event of complement activation prevents antibody-induced fetal loss. In this issue of the JCI, the study by Redecha et al. clarifies that in mice, the contribution of TF to this pathogenic mechanism is independent of its role in coagulation and thrombosis, but involves inflammatory signaling through the receptor PAR2 (see the related article beginning on page 3453). The study not only sheds light on a critical effector mechanism of aPL-induced fetal loss, but also suggests that treatment with statins, which decrease TF and PAR2 expression, may hold promise as a therapeutic approach to antiphospholipid syndrome-associated pregnancy complications.
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Registered trials
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