ArticleHaematologica2025
Different inflammatory, fibrotic, and immunological signatures between pre-fibrotic and overt primary myelofibrosis.
Article in Haematologica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Megakaryocytes in myelofibrosis: mechanisms of fibrotic niche remodeling and therapeutic implications.Biomarker research · 2026Review
- Inhibition of RhoA-mediated secretory autophagy in megakaryocytes mitigates myelofibrosis in mice.Nature communications · 2026Article
- Clonal Metamorphosis: Deconstructing MPN Evolution with Single-Cell and Spatial Multi-Omics.Clinical and experimental medicine · 2026Review
- Myeloid Malignancies Beyond the Cell: Targeting the Tumour Microenvironment with Next-Generation Immunotherapies.Cancers · 2026Review
- Hematopoietic JAK2V617F mutation-induced reprogramming of blood and bone marrow megakaryocytes.Blood advances · 2026Article
- Prospects of Chimeric Antigen Receptor T-Cell Therapy in Myelofibrosis: From Immunopathogenesis to Therapeutic Strategies.Cancers · 2026Review
- Monocyte Involvement in the Pathogenesis of Myeloproliferative Neoplasms.International journal of molecular sciences · 2025Review
- Primary myelofibrosis progression: a game of cellular telephone.Haematologica · 2025Article
- Identification of GBN5 as a molecular biomarker of pan-cancer species by integrated multi-omics analysis.Discover oncology · 2025Article
- Chronic Inflammation in Primary Myelofibrosis: In-Depth Insights Into Pathogenesis and Promising Anti-Inflammatory Therapeutic Strategies.Mediators of inflammation · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary myelofibrosis (PMF) is a myeloid proliferative neoplasm (MPN) characterized by bone marrow fibrosis. Pre-fibrotic PMF (pre-PMF) progresses to overt PMF. Megakaryocytes play a primary role in PMF; however, the functions of megakaryocyte subsets and those of other hematopoietic cells during PMF progression remain unclear. We, therefore, analyzed bone marrow aspirates in cases of pre-PMF, overt PMF, and other MPN using single-cell RNA sequencing. We identified 14 cell types with subsets, including hematopoietic stem and progenitor cells (HSPC) and megakaryocytes. HSPC in overt PMF were megakaryocyte-biased and inflammation/fibrosis-enriched. Among megakaryocytes, the epithelial-mesenchymal transition (EMT)-enriched subset was abruptly increased in overt PMF. Megakaryocytes in non-fibrotic/non-PMF MPN were megakaryocyte differentiation-enriched, whereas those in fibrotic/non-PMF MPN were inflammation/fibrosis-enriched. Overall, the inflammation/fibrosis signatures of the HSPC, megakaryocyte, and CD14+ monocyte subsets increased from pre-PMF to overt PMF. Cytotoxic and dysfunctional scores also increased in T and NK cells. Clinically, megakaryocyte and HSPC subsets with high inflammation/fibrosis signatures were frequent in the patients with peripheral blood blasts ≥1%. Single-cell RNA-sequencing predicted higher cellular communication of megakaryocyte differentiation, inflammation/fibrosis, immunological effector/dysfunction, and tumor-associated signaling in overt PMF than in pre-PMF. However, no decisive subset emerged during PMF progression. Our study demonstrated that HSPC, monocytes, and lymphoid cells contribute to the progression of PMF, and subset specificity existed regarding inflammation/fibrosis and immunological dysfunction. PMF progression may depend on alterations of multiple cell types, and EMT-enriched megakaryocytes may be potential targets for diagnosing and treating the progression.
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