ArticleLeukemia2023
Inhibition of ERK1/2 signaling prevents bone marrow fibrosis by reducing osteopontin plasma levels in a myelofibrosis mouse model.
Article in Leukemia, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- A stem and progenitor cell-derived gene expression signature is prognostic for survival in myelofibrosis.Blood · 2026Article
- Integrated analysis of single-cell RNA sequencing, transcriptomics, and thermal proteome profiling identifies PLCG1 as the therapeutic target of isopimpinellin in treating rheumatoid arthritis.Cellular & molecular biology letters · 2026Article
- Combined MEK and JAK inhibition reduces osteopontin plasma level and bone marrow fibrosis in a myelofibrosis mouse model.Blood cancer journal · 2025Article
- CD44 Participates to Extramedullary Haematopoiesis Onset by Mediating the Interplay Between Monocytes and Haematopoietic Stem Cells in Myelofibrosis.Journal of cellular and molecular medicine · 2025Article
- Targeted Therapies in Myelofibrosis: Present Landscape, Ongoing Studies, and Future Perspectives.American journal of hematology · 2025Review
- Tumor cell-derived osteopontin promotes tumor fibrosis indirectly via tumor-associated macrophages.Journal of translational medicine · 2025Article
- Use of Mesenchymal Stem Cell-Targeting 3WJ Nanoparticles and Reported Specific Delivery of Anti-miRNA 138 to Treat Osteoporosis.ACS omega · 2025Article
- Lactate accumulation promotes immunosuppression and fibrotic transformation of bone marrow microenvironment in myelofibrosis.Journal of translational medicine · 2025Article
- Differential contribution for ERK1 and ERK2 kinases in BRAFCell death and differentiation · 2024Article
- Immunoregulatory Roles of Osteopontin in Diseases.Nutrients · 2024Review
- HDAC7 drives glioblastoma to a mesenchymal-like state via LGALS3-mediated crosstalk between cancer cells and macrophages.Theranostics · 2024Article
- Exploring the Molecular Landscape of Myelofibrosis, with a Focus on Ras and Mitogen-Activated Protein (MAP) Kinase Signaling.Cancers · 2023Review
- Recent advances in therapies for primary myelofibrosis.Faculty reviews · 2023Review
Corrections and comments
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Authors and funding
25 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clonal myeloproliferation and development of bone marrow (BM) fibrosis are the major pathogenetic events in myelofibrosis (MF). The identification of novel antifibrotic strategies is of utmost importance since the effectiveness of current therapies in reverting BM fibrosis is debated. We previously demonstrated that osteopontin (OPN) has a profibrotic role in MF by promoting mesenchymal stromal cells proliferation and collagen production. Moreover, increased plasma OPN correlated with higher BM fibrosis grade and inferior overall survival in MF patients. To understand whether OPN is a druggable target in MF, we assessed putative inhibitors of OPN expression in vitro and identified ERK1/2 as a major regulator of OPN production. Increased OPN plasma levels were associated with BM fibrosis development in the Romiplostim-induced MF mouse model. Moreover, ERK1/2 inhibition led to a remarkable reduction of OPN production and BM fibrosis in Romiplostim-treated mice. Strikingly, the antifibrotic effect of ERK1/2 inhibition can be mainly ascribed to the reduced OPN production since it could be recapitulated through the administration of anti-OPN neutralizing antibody. Our results demonstrate that OPN is a novel druggable target in MF and pave the way to antifibrotic therapies based on the inhibition of ERK1/2-driven OPN production or the neutralization of OPN activity.
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