ArticleJournal of thrombosis and haemostasis : JTH2021
The contribution of TFPIα to the hemostatic response to injury in mice.
Article in Journal of thrombosis and haemostasis : JTH, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Volume electron microscopy reveals heterogeneity of the hemostatic response in veins and arteries.Blood advances · 2026Article
- Placental Vascular Defects and Embryonic Lethality Triggered by TFPIα Deficiency in Factor V Leiden Mice.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- TFPIα anticoagulant function is highly dependent on protein S in vivo.Science advances · 2024Article
- Platelet tissue factor pathway inhibitor-α dampens cardiac thrombosis and associated fibrosis in mice.Journal of thrombosis and haemostasis : JTH · 2023Article
- TFPI inhibits breast cancer progression by suppressing ERK/p38 MAPK signaling pathway.Genes & genomics · 2022Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundTissue factor pathway inhibitor (TFPI) is an essential regulator of coagulation, limiting thrombin generation and preventing thrombosis. In humans and mice, TFPIα is the sole isoform present in platelets.
objectiveHere, we asked whether TFPIα, because of its release from platelets at sites of injury, has a unique role in limiting the hemostatic response.
methodsTFPIα-mutant (Tfpi
resultsTfpi
conclusionLoss of TFPIα expression does not produce a global prothrombotic state in mice. Platelet TFPIα is expected to be released or displayed in a focal manner at the site of injury, potentially accumulating to high concentrations in the narrow gaps between platelets. If so, the data from the vascular injury models studied here indicate this is not essential for a normal hemostatic response in mice.
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Registered trials
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