ArticleTranslational stroke research2012
Inhibition of Factor XII-Mediated Activation of Factor XI Provides Protection Against Experimental Acute Ischemic Stroke in Mice.
Article in Translational stroke research, 2012. 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 56 citations in OpenAlex.
- Contact Activation Inhibitor and Factor XI Antibody, AB023, Produces Safe, Dose-Dependent Anticoagulation in a Phase 1 First-In-Human Trial.Arteriosclerosis, thrombosis, and vascular biology · 2019Trial
- FXI and FXII in experimental stroke and FXI in clinical stroke trials.Neurological research and practice · 2026Review
- Factor XI Inhibition for Ischemic Stroke Secondary Prevention: Pharmacology, Clinical Evidence, and Future Directions.Journal of clinical pharmacology · 2026Review
- Integrative proteogenomic analyses identify plasma proteins that impact the risk of ischemic stroke.Communications medicine · 2026Article
- Beyond traditional anticoagulants: exploring the future of thromboembolism treatment with FXI inhibitors.Frontiers in immunology · 2026Review
- Identification of Six Potential Therapeutic Targets Common to Ischemic Stroke and Vascular Dementia: Genetic Insights From an Integrated Bioinformatics Analysis.Brain and behavior · 2025Article
- Proteome-wide Mendelian randomization and colocalization analysis identify therapeutic targets for stroke.BMC neurology · 2025Article
- Coagulation factor XI regulates endothelial cell permeability and barrier function in vitro and in vivo.Blood · 2024Article
- Biology of factor XI.Blood · 2024Review
- Review
- New Directions in Infection-Associated Ischemic Stroke.Journal of clinical neurology (Seoul, Korea) · 2024Review
- Activation of coagulation FXI promotes endothelial inflammation and amplifies platelet activation in a nonhuman primate model of hyperlipidemia.Research and practice in thrombosis and haemostasis · 2024Article
- Pharmacological targeting of coagulation factor XI attenuates experimental autoimmune encephalomyelitis in mice.Metabolic brain disease · 2023Article
- Blood Coagulation and Beyond: Position Paper from the Fourth Maastricht Consensus Conference on Thrombosis.Thrombosis and haemostasis · 2023Article
- Targeting the contact system in a rabbit model of extracorporeal membrane oxygenation.Blood advances · 2023Article
- Factor XII contributes to thrombotic complications and vaso-occlusion in sickle cell disease.Blood · 2023Article
- 6-(Arylaminomethyl) Isoquinolines as Enzyme Inhibitors and Their Preparation: A Patent Highlight of Factor XIIa Inhibitors.Cardiovascular & hematological agents in medicinal chemistry · 2023Article
- Novel contact-kinin inhibitor sylvestin targets thromboinflammation and ameliorates ischemic stroke.Cellular and molecular life sciences : CMLS · 2022Article
- Intrinsic Pathway of Coagulation and Thrombosis.Arteriosclerosis, thrombosis, and vascular biology · 2019Review
- Plasma contact factors as therapeutic targets.Blood reviews · 2018Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Blood coagulation factor XI (FXI) is an established risk factor for acute ischemic stroke (AIS) and thrombosis, but is also needed for normal hemostasis. Contact factor XII (FXII), an upstream activator of FXI, also contributes to experimental stroke, but is not required for hemostasis. We investigated whether selectively inhibiting FXII-mediated FXI activation, while leaving other FXI and FXII functions intact, could improve the outcome of experimental AIS in mice. Twenty-four hours before induction of AIS by placement of a filament into the internal carotid artery for 60 min, mice were anticoagulated with an antibody directed against the apple 2 domain of FXI. This antibody selectively reduces the prothrombotic activation of FXI by FXIIa but does not affect activated FXI or hemostatic activation of FXI by thrombin, thus leaving hemostasis intact in mice and primates. In this model of AIS/reperfusion injury, mice that received the antibody before AIS displayed less ischemic damage, manifested as reduced cerebral infarction and fibrin deposition (thrombosis), increased cortical reperfusion, and improved neurological behavior. Further, the antibody-anticoagulated mice had no detectable hemostasis impairment. Consistent with the neuroprotective phenotype of FXII-deficient mice, our data suggest that a single molecular event, FXII-mediated FXI activation, contributes to the development of experimental AIS.
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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.