ArticleBlood2024
PF4 activates the c-Mpl-Jak2 pathway in platelets.
Article in Blood, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 40 citations in OpenAlex.
- Insights Into the Role of Platelet Factor 4 in Neurodegenerative Diseases.CNS neuroscience & therapeutics · 2026Review
- Gut Microbiota Regulates Systemic Inflammatory Response and Compensatory Anti-Inflammatory Response Syndromes by Targeting PF4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Generation and single-cell characterization of functional megakaryocytes derived from umbilical cord blood.Stem cell research & therapy · 2026Article
- Engineering platelets as cancer therapeutics.Nature reviews. Clinical oncology · 2026Review
- Research progress on blood therapy for anti-aging.Journal of advanced research · 2026Review
- Article
- Platelets in systemic lupus erythematosus: from hemostatic allies to pathogenic drivers.Frontiers in immunology · 2026Review
- Platelet factor 4 in cognitive, immune and hematopoietic aging: emerging evidence and translational challenges.Frontiers in immunology · 2026Review
- Glycoprotein VI is a receptor for the PF4/anti-PF4 IgG complex and contributes to platelet activation in heparin-induced thrombocytopenia (HIT).Journal of thrombosis and haemostasis : JTH · 2025Article
- An αIIbβ3 ligand-mimetic murine monoclonal antibody that produces platelet activation by engaging the FcγIIa receptor.Blood advances · 2025Article
- Accurate Delivery of Mesenchymal Stem Cell Spheroids With Platelet-Rich Fibrin Shield: Enhancing Survival and Repair Functions of Sp-MSCs in Diabetic Wound Healing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Review
- Article
- Platelet spleen tyrosine kinase is a key regulator of anti-PF4 antibody-induced immunothrombosis.Blood advances · 2025Article
- Anti-Platelet factor 4 immunothrombosis-not just heparin and vaccine triggers.Research and practice in thrombosis and haemostasis · 2025Review
- Editorial: Similarities and differences between cellular and molecular mechanisms of normal brain aging and neurodegeneration.Frontiers in aging neuroscience · 2025Article
- Association between the platelet-to-albumin ratio and 28-day all-cause mortality in critically ill patients with Pulmonary embolism: a retrospective cohort study and predictive model establishment based on machine learning.Frontiers in medicine · 2025Article
- Advances in our understanding of anti-PF4 related immunothrombosis.Frontiers in immunology · 2025Review
- Alterations in visible light exposure modulate platelet function and regulate thrombus formation.Journal of thrombosis and haemostasis : JTH · 2025Article
- Platelet signaling in immune landscape: comprehensive mechanism and clinical therapy.Biomarker research · 2024Review
Corrections and comments
- Commented on by
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
abstractPlatelet factor 4 (PF4) is an abundant chemokine that is released from platelet α-granules on activation. PF4 is central to the pathophysiology of vaccine-induced immune thrombocytopenia and thrombosis (VITT) in which antibodies to PF4 form immune complexes with PF4, which activate platelets and neutrophils through Fc receptors. In this study, we show that PF4 binds and activates the thrombopoietin receptor, cellular myeloproliferative leukemia protein (c-Mpl), on platelets. This leads to the activation of Janus kinase 2 (JAK2) and phosphorylation of signal transducer and activator of transcription (STAT) 3 and STAT5, leading to platelet aggregation. Inhibition of the c-Mpl-JAK2 pathway inhibits platelet aggregation to PF4, VITT sera, and the combination of PF4 and IgG isolated from VITT patient plasma. The results support a model in which PF4-based immune complexes activate platelets through binding of the Fc domain to FcγRIIA and PF4 to c-Mpl.
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.