ReviewSeminars in thrombosis and hemostasis2018
Inhibition of Factors XI and XII for Prevention of Thrombosis Induced by Artificial Surfaces.
Review in Seminars in thrombosis and hemostasis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled 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.
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
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- Factor XII-A New Therapeutic Target? A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Factor XI inhibitors for the prevention and treatment of venous and arterial thromboembolism.Nature reviews. Cardiology · 2025Review
- Coagulation factor XII haploinsufficiency is protective against venous thromboembolism in a population-scale multidimensional analysis.Nature communications · 2025Article
- Factor XII Structure-Function Relationships.Seminars in thrombosis and hemostasis · 2024Review
- Thrombogenicity of biodegradable metals.Bioactive materials · 2024Article
- Pharmacologic targeting of coagulation factors XII and XI by monoclonal antibodies reduces thrombosis in nitinol stents under flow.Journal of thrombosis and haemostasis : JTH · 2024Article
- Review
- Factor XI Inhibitors: A New Horizon in Anticoagulation Therapy.Cardiology and therapy · 2024Review
- Abelacimab: A leap forward in anticoagulation with FXI and FXIa Inhibition.Current research in pharmacology and drug discovery · 2024Review
- Hereditary angioedema and thrombosis.Blood · 2023Article
- Targeting the contact system in a rabbit model of extracorporeal membrane oxygenation.Blood advances · 2023Article
- The new in anticoagulation: factor XI inhibitors.European heart journal supplements : journal of the European Society of Cardiology · 2023Article
- Triazol-1-yl Benzamides Promote Anticoagulant ActivityCardiovascular & hematological agents in medicinal chemistry · 2023Article
- Mechanisms involved in hereditary angioedema with normal C1-inhibitor activity.Frontiers in physiology · 2023Review
- 3-(Cardiovascular & hematological agents in medicinal chemistry · 2023Article
- Amide-functionalized 1,2,4-Triazol-5-amines as Covalent Inhibitors of Blood Coagulation Factor XIIa and Thrombin.ACS pharmacology & translational science · 2022Article
- Associations between coagulation factor XII, coagulation factor XI, and stability of venous thromboembolism: A case-control study.World journal of clinical cases · 2022Article
- Validation of lipid-related therapeutic targets for coronary heart disease prevention using human genetics.Nature communications · 2021Article
- Article
- The SARS-CoV-2/Receptor Axis in Heart and Blood Vessels: A Crisp Update on COVID-19 Disease with Cardiovascular Complications.Viruses · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Exposure of blood to a variety of artificial surface induces contact activation, a process that contributes to the host innate response to foreign substances. On the foreign surface, the contact factors, factor XII (FXII), and plasma prekallikrein undergo reciprocal conversion to their fully active protease forms (FXIIa and α-kallikrein, respectively) by a process supported by the cofactor high-molecular-weight kininogen. Contact activation can trigger blood coagulation by conversion of factor XI (FXI) to the protease FXIa. There is interest in developing therapeutic inhibitors to FXIa and FXIIa because these activated factors can contribute to thrombosis in certain situations. Drugs targeting these proteases may be particularly effective in thrombosis triggered by exposure of blood to the surfaces of implantable medical devices. Here, we review clinical data supporting roles for FXII and FXI in thrombosis induced by medical devices, and preclinical data suggesting that therapeutic targeting of these proteins may limit surface-induced thrombosis.
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.