ArticleBlood2009
Role of tissue factor in a mouse model of thrombotic microangiopathy induced by antiphospholipid antibodies.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
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.
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Who cites it
34 citing papers in PubMed, 80 citations in OpenAlex.
- Association of IgA antiphospholipid antibodies with hypercoagulability and inflammation in antiphospholipid syndrome.Journal of thrombosis and thrombolysis · 2026Observational
- Complement activation in secondary thrombotic microangiopathies.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Review
- Perspective on Renal Involvement in Antiphospholipid Syndrome: Implications for Diagnosis, Pathogenesis, and Treatment.Journal of clinical medicine · 2025Review
- The Many Faces of Protease-Activated Receptor 2 in Kidney Injury.Biomedicines · 2025Review
- Mechanism of antiphospholipid antibody-mediated thrombosis in antiphospholipid syndrome.Frontiers in immunology · 2025Review
- Kidney whole-transcriptome profiling in primary antiphospholipid syndrome reveals complement, interferons and NETs-related gene expression.Rheumatology (Oxford, England) · 2024Article
- Targeting the tissue factor coagulation initiation complex prevents antiphospholipid antibody development.Blood · 2024Article
- Inhibiting Tyrosine Kinase 2 Ameliorates Antiphospholipid Syndrome Nephropathy.Mediators of inflammation · 2024Article
- Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of Anti-C5a Antibody BDB-001 for Severe COVID-19: A Randomized, Double-Blind, Placebo-Controlled Phase 1 Clinical Trial in Healthy Chinese Adults.Infectious diseases and therapy · 2023Article
- Emerging Therapies in Antiphospholipid Syndrome.Transfusion medicine reviews · 2022Review
- COVID-19 associated coagulopathy: Mechanisms and host-directed treatment.The American journal of the medical sciences · 2022Review
- A guide to immunotherapy for COVID-19.Nature medicine · 2022Review
- Anti-C5a antibody IFX-1 (vilobelimab) treatment versus best supportive care for patients with severe COVID-19 (PANAMO): an exploratory, open-label, phase 2 randomised controlled trial.The Lancet. Rheumatology · 2020Article
- Is the COVID-19 thrombotic catastrophe complement-connected?Journal of thrombosis and haemostasis : JTH · 2020Review
- Management of Non-criteria Manifestations in Antiphospholipid Syndrome.Current rheumatology reports · 2020Review
- COVID-19, Antiphospholipid Antibodies, and Catastrophic Antiphospholipid Syndrome: A Possible Association?Clinical medicine insights. Arthritis and musculoskeletal disorders · 2020Review
- Protease-activated receptor 2 protects against VEGF inhibitor-induced glomerular endothelial and podocyte injury.Scientific reports · 2019Article
- Thrombotic microangiopathy associated with anticardiolipin antibody in a kidney transplant recipient with polycythemia.CEN case reports · 2019Article
- Renal involvement in antiphospholipid syndrome.Rheumatology international · 2018Review
- Obstetric Anti-phospholipid Syndrome: State of the Art.Current rheumatology reports · 2018Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Using different mouse monoclonal and human antiphospholipid (aPL) antibodies, we developed a new animal model of renal injury that shares many features with thrombotic microangiopathy (TMA). We found that more than 1 mechanism/signaling pathway is involved in glomerular injury induced by aPL antibodies in this model. Both complement-dependent and complement-independent pathways were identified that lead to glomerular endothelial cell damage and renal function impairment. We also found that C5a-C5aR interaction is a crucial step for the activation of the coagulation cascade and glomerular injury induced by complement-activating antibodies. In addition, our studies demonstrated complement-independent mechanisms in which reactivity with beta(2) glycoprotein I (beta2GPI) plays an important role in aPL-induced glomerular damage and renal failure. Independently of the mechanism responsible for aPL-induced TMA, mice that express low levels of tissue factor (TF) were protected from glomerular injury. That genetic reduction of TF prevents renal injury induced by different aPL antibodies indicates that TF is a common mediator of glomerular damage and a possible target for selective pharmacologic intervention. Treatment with pravastatin, which down-regulates glomerular TF synthesis, prevents aPL-induced TMA in this mouse model, thus emphasizing that targeting TF might be a good therapeutic intervention in patients with TMA.
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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.