ArticleBlood cells, molecules & diseases2015
Activation of non-canonical TGF-β1 signaling indicates an autoimmune mechanism for bone marrow fibrosis in primary myelofibrosis.
Article in Blood cells, molecules & diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Shared and Tissue-Specific Expression Signatures between Bone Marrow from Primary Myelofibrosis and Essential Thrombocythemia.Experimental hematology · 2019Trial
- Folate metabolism in myelofibrosis: a missing key?Annals of hematology · 2025Review
- Megakaryocyte Secreted Factors Regulate Bone Marrow Niche Cells During Skeletal Homeostasis, Aging, and Disease.Calcified tissue international · 2023Review
- TGF-β signaling in myeloproliferative neoplasms contributes to myelofibrosis without disrupting the hematopoietic niche.The Journal of clinical investigation · 2022Article
- Genetics and Pathogenetic Role of Inflammasomes in Philadelphia Negative Chronic Myeloproliferative Neoplasms: A Narrative Review.International journal of molecular sciences · 2021Review
- Interleukin-17-induced neutrophil extracellular traps mediate resistance to checkpoint blockade in pancreatic cancer.The Journal of experimental medicine · 2020Article
- Role of Inflammatory Factors during Disease Pathogenesis and Stem Cell Transplantation in Myeloproliferative Neoplasms.Cancers · 2020Review
- Novel targets to cure primary myelofibrosis from studies on Gata1IUBMB life · 2020Review
- Monocytic Myeloid Derived Suppressor Cells in Hematological Malignancies.International journal of molecular sciences · 2019Review
- Novel strategies for the treatment of myelofibrosis driven by recent advances in understanding the role of the microenvironment in its etiology.F1000Research · 2019Review
- GATA1 insufficiencies in primary myelofibrosis and other hematopoietic disorders: consequences for therapy.Expert review of hematology · 2018Review
- Megakaryocyte Contribution to Bone Marrow Fibrosis: many Arrows in the Quiver.Mediterranean journal of hematology and infectious diseases · 2018Review
- The thrombopoietin/MPL axis is activated in the Gata1Blood cancer journal · 2017Article
- Mathematical modelling as a proof of concept for MPNs as a human inflammation model for cancer development.PloS one · 2017Article
- Mesenchymal Cell Reprogramming in Experimental MPLW515L Mouse Model of Myelofibrosis.PloS one · 2017Article
- Preclinical rationale for TGF-β inhibition as a therapeutic target for the treatment of myelofibrosis.Experimental hematology · 2016Article
- Hematopoietic Stem Cell Regulation by Type I and II Interferons in the Pathogenesis of Acquired Aplastic Anemia.Frontiers in immunology · 2016Review
- MPNs as Inflammatory Diseases: The Evidence, Consequences, and Perspectives.Mediators of inflammation · 2015Review
- A novel interaction between megakaryocytes and activated fibrocytes increases TGF-β bioavailability in the Gata1(low) mouse model of myelofibrosis.American journal of blood research · 2015Article
- Inflammation as a Keystone of Bone Marrow Stroma Alterations in Primary Myelofibrosis.Mediators of inflammation · 2015Review
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Primary myelofibrosis (PMF) is characterized by megakaryocyte hyperplasia, dysplasia and death with progressive reticulin/collagen fibrosis in marrow and hematopoiesis in extramedullary sites. The mechanism of fibrosis was investigated by comparing TGF-β1 signaling of marrow and spleen of patients with PMF and of non-diseased individuals. Expression of 39 (23 up-regulated and 16 down-regulated) and 38 (8 up-regulated and 30 down-regulated) TGF-β1 signaling genes was altered in the marrow and spleen of PMF patients, respectively. Abnormalities included genes of TGF-β1 signaling, cell cycling and abnormal in chronic myeloid leukemia (EVI1 and p21(CIP)) (both marrow and spleen) and Hedgehog (marrow only) and p53 (spleen only) signaling. Pathway analyses of these alterations predict an increased osteoblast differentiation, ineffective hematopoiesis and fibrosis driven by non-canonical TGF-β1 signaling in marrow and increased proliferation and defective DNA repair in spleen. Since activation of non-canonical TGF-β1 signaling is associated with fibrosis in autoimmune diseases, the hypothesis that fibrosis in PMF results from an autoimmune process triggered by dead megakaryocytes was tested by determining that PMF patients expressed plasma levels of mitochondrial DNA and anti-mitochondrial antibodies greater than normal controls. These data identify autoimmunity as a possible cause of marrow fibrosis in PMF.
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