ReviewCurrent rheumatology reports2010
Impaired fibrinolysis in the antiphospholipid syndrome.
Review in Current rheumatology reports, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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.
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.
Who cites it
30 citing papers in PubMed, 89 citations in OpenAlex.
- Presence of antiphospholipid antibody is a risk factor in thrombotic events in patients with antiphospholipid syndrome or relevant diseases.International journal of hematology · 2013Trial
- Antiphospholipid antibodies and cardiovascular thrombosis.Nature reviews. Cardiology · 2026Review
- The role of neutrophil extracellular traps in antiphospholipid syndrome.Frontiers in immunology · 2026Review
- Coronary plaque healing: a safety net or a hazard indicator?Journal of thrombosis and thrombolysis · 2026Review
- Pathogenic and Regulatory Roles of Fibrinolytic Factors in Autoimmune Diseases.Current issues in molecular biology · 2025Review
- Thromboprophylaxis in patients admitted to inpatient rehabilitation and skilled nursing facilities post total joint arthroplasty.Archives of orthopaedic and trauma surgery · 2025Article
- Antiphospholipid Antibodies as Key Players in Systemic Lupus Erythematosus: The Relationship with Cytokines and Immune Dysregulation.International journal of molecular sciences · 2024Review
- Evaluating complement dysregulation in livedoid vasculopathy using a functional assay.Blood advances · 2023Article
- A Novel Thrombolytic Regimen for Mechanical Prosthetic Valve Thrombosis in a Patient With Antiphospholipid Syndrome.Cureus · 2022Article
- Article
- Assessing Plasmin Generation in Health and Disease.International journal of molecular sciences · 2021Review
- Renal microvascular lesions in lupus nephritis.Renal failure · 2020Review
- Complement in the Pathophysiology of the Antiphospholipid Syndrome.Frontiers in immunology · 2019Review
- Renal involvement in antiphospholipid syndrome.Rheumatology international · 2018Review
- Obstetric Anti-phospholipid Syndrome: State of the Art.Current rheumatology reports · 2018Review
- The Differences Between Childhood and Adult Onset Antiphospholipid Syndrome.Frontiers in pediatrics · 2018Review
- Immunological Tolerance, Pregnancy, and Preeclampsia: The Roles of Semen Microbes and the Father.Frontiers in medicine · 2017Article
- Dysfunction in the coagulation system and schizophrenia.Translational psychiatry · 2016Review
- The journey of antiphospholipid antibodies from cellular activation to antiphospholipid syndrome.Current rheumatology reports · 2015Review
- Fibrinolysis and the control of blood coagulation.Blood reviews · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The antiphospholipid syndrome (APS) is characterized by venous and/or arterial thrombosis, or recurrent fetal loss, in the presence of antiphospholipid antibodies (APL). The pathogenesis of APS is multifaceted and involves numerous mechanisms including activation of endothelial cells, monocytes, and/or platelets; inhibition of natural anticoagulant pathways such as protein C, tissue factor inhibitor, and annexin A5; activation of the complement system; and impairment of the fibrinolytic system. Fibrinolysis--the process by which fibrin thrombi are remodeled and degraded--involves the conversion of plasminogen to plasmin by tissue plasminogen activator (tPA) or urokinase-type plasminogen activator, and is tightly regulated. Although the role of altered fibrinolysis in patients with APS is relatively understudied, several reports suggest that deficient fibrinolytic activity may contribute to the pathogenesis of disease in these patients. This article discusses the function of the fibrinolytic system and reviews studies that have reported alterations in fibrinolytic pathways that may contribute to thrombosis in patients with APL. Some of these mechanisms include elevations in plasminogen activator inhibitor-1 levels, inhibitory antibodies against tPA or other components of the fibrinolytic system, antibodies against annexin A2, and finally, antibodies to beta(2)-glycoprotein-I (beta(2)GPI) that block the ability of beta(2)GPI to stimulate tPA-mediated plasminogen activation.
Indexed as
Identifiers
What OpenQuestion holds
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.