ArticleBlood2020
Increased CXCL4 expression in hematopoietic cells links inflammation and progression of bone marrow fibrosis in MPN.
Article in Blood, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05423691 (Phase Ib, Open-label Study of Add on Therapy With CK0804 in Participants With Myelofibrosis, With Suboptimal Response to Ruxolitinib), which is not on this map. Cited by 60 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.
Phase Ib, Open-label Study of Add on Therapy With CK0804 in Participants With Myelofibrosis, With Suboptimal Response to Ruxolitinib
Who cites it
60 citing papers in PubMed, 98 citations in OpenAlex.
- Fufang Huangbo Formula mitigates myeloproliferative neoplasms by activating p53/p21 signaling axis and inhibiting STAT3 and NF-κB signaling pathways.Pharmaceutical science advances · 2026Article
- Non-invasive multiparametric characterization of essential thrombocythemia, premyelofibrosis, and overt myelofibrosis.Leukemia · 2026Article
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- Inflammatory and Immune Microenvironment in Myeloproliferative Neoplasms: Pathogenic Mechanisms and Therapeutic Opportunities.Cancers · 2026Review
- Inhibition of RhoA-mediated secretory autophagy in megakaryocytes mitigates myelofibrosis in mice.Nature communications · 2026Article
- The inflammatory/fibrotic axis across organs: myelofibrosis as a model of reversibility.JCI insight · 2026Review
- Immunomodulatory Agents and Factors in Poor Hematopoietic Stem Cell Mobilization: Current Strategies and Future Prospects.Stem cell reviews and reports · 2026Review
- Research progress on blood therapy for anti-aging.Journal of advanced research · 2026Review
- The Intricate Dance Between Inflammation and Myeloproliferative Neoplasms: From Origins to Outcomes.Current hematologic malignancy reports · 2026Review
- Article
- CXCL4 and CXCL4L1 activate human macrophage via TLR4 signaling to modulate inflammatory responses.Cell insight · 2026Article
- Non-invasive detection of bone marrow fibrosis in myeloproliferative neoplasms using cell-free RNA.iScience · 2026Article
- Platelet factor 4 in cognitive, immune and hematopoietic aging: emerging evidence and translational challenges.Frontiers in immunology · 2026Review
- Profibrotic macrophage-derived CXCL4 promotes pericyte-to-myofibroblast transition after spinal cord injury.Journal of orthopaedic translation · 2026Article
- Combined MEK and JAK inhibition reduces osteopontin plasma level and bone marrow fibrosis in a myelofibrosis mouse model.Blood cancer journal · 2025Article
- Inhibiting the alarmin-driven hematopoiesis-stromal cell crosstalk in primary myelofibrosis ameliorates bone marrow fibrosis.HemaSphere · 2025Article
- SPI1 triggers the formation of neutrophil extracellular traps in multiple sclerosis through CXCL4.Journal of molecular histology · 2025Article
- Article
- Targeted Therapies in Myelofibrosis: Present Landscape, Ongoing Studies, and Future Perspectives.American journal of hematology · 2025Review
- Malignant JAK-signaling: at the interface of inflammation and malignant transformation.Leukemia · 2025Review
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Authors and funding
21 authors at 9 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary myelofibrosis (PMF) is a myeloproliferative neoplasm (MPN) that leads to progressive bone marrow (BM) fibrosis. Although the cellular mutations involved in the pathogenesis of PMF have been extensively investigated, the sequential events that drive stromal activation and fibrosis by hematopoietic-stromal cross-talk remain elusive. Using an unbiased approach and validation in patients with MPN, we determined that the differential spatial expression of the chemokine CXCL4/platelet factor-4 marks the progression of fibrosis. We show that the absence of hematopoietic CXCL4 ameliorates the MPN phenotype, reduces stromal cell activation and BM fibrosis, and decreases the activation of profibrotic pathways in megakaryocytes, inflammation in fibrosis-driving cells, and JAK/STAT activation in both megakaryocytes and stromal cells in 3 murine PMF models. Our data indicate that higher CXCL4 expression in MPN has profibrotic effects and is a mediator of the characteristic inflammation. Therefore, targeting CXCL4 might be a promising strategy to reduce inflammation in PMF.
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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.