ArticleJournal of thrombosis and haemostasis : JTH2014
Targeting the anionic region of human protease-activated receptor 4 inhibits platelet aggregation and thrombosis without interfering with hemostasis.
Article in Journal of thrombosis and haemostasis : JTH, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 35 citations in OpenAlex.
- Endothelial protease-activated receptor 4: impotent or important?Frontiers in cardiovascular medicine · 2025Review
- Murine cadherin-6 mediates thrombosis in vivo in a platelet-independent manner.Research and practice in thrombosis and haemostasis · 2021Article
- The domino effect triggered by the tethered ligand of the protease activated receptors.Thrombosis research · 2020Review
- Using PAR4 Inhibition as an Anti-Thrombotic Approach: Why, How, and When?International journal of molecular sciences · 2019Review
- The role of coagulation and platelets in colon cancer-associated thrombosis.American journal of physiology. Cell physiology · 2019Article
- A function-blocking PAR4 antibody is markedly antithrombotic in the face of a hyperreactive PAR4 variant.Blood advances · 2018Article
- Protease-Activated Receptor 4 (PAR4): A Promising Target for Antiplatelet Therapy.International journal of molecular sciences · 2018Review
- PAR4 (Protease-Activated Receptor 4): PARticularly Important 4 Antiplatelet Therapy.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Optimizing the presentation of bleeding and thrombosis data: Responding to censored data using Kaplan-Meier curves.Thrombosis research · 2017Article
- Opportunities for therapeutic antibodies directed at G-protein-coupled receptors.Nature reviews. Drug discovery · 2017Review
- Production and characterization of polyclonal antibodies to human recombinant domain B-free antihemophilic factor VIII.Turkish journal of biology = Turk biyoloji dergisi · 2017Article
- Protease-activated receptor 4: from structure to function and back again.British journal of pharmacology · 2016Review
- Ferric Chloride-induced Murine Thrombosis Models.Journal of visualized experiments : JoVE · 2016Article
- Protease-activated receptors in hemostasis.Blood · 2016Review
- Chronic, not acute, skin-specific inflammation promotes thrombosis in psoriasis murine models.Journal of translational medicine · 2015Article
- Development and characterization of monoclonal antibodies against Protease Activated Receptor 4 (PAR4).Thrombosis research · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHuman platelet activation and aggregation is a complex process. To date, many therapies have been developed targeting proteins that mediate this process to prevent unwanted activation. However, the current standard of care for acute coronary syndromes still has limitations, including bleeding risk.
objectiveTo evaluate the protease-activated receptor 4 (PAR4) anionic cluster as a viable antiplatelet target by using a polyclonal antibody (CAN12).
methodsWe used western blotting, aggregation and secretion ex vivo to evaluate the ability of CAN12 to interact with PAR4 and inhibit platelet activation. The effects of CAN12 in vivo were evaluated with the Rose Bengal arterial thrombosis model and two models of hemostasis.
resultsCAN12 was able to interact with human PAR4 and delay PAR4 cleavage. In addition, CAN12 inhibited thrombin-induced human platelet aggregation and secretion in a dose-dependent manner. The specificity of CAN12 was agonist-dependent. In vivo, we determined that CAN12 was able to inhibit arterial thrombosis, and, using two independent methods, we found that CAN12 did not influence hemostasis.
conclusionTargeting the extracellular anionic cluster on PAR4 is a viable novel strategy as an antiplatelet therapy.
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.