ArticleJCI insight2020
Increased FGF-23 levels are linked to ineffective erythropoiesis and impaired bone mineralization in myelodysplastic syndromes.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 26 citations in OpenAlex.
- Bone health in myelodysplastic neoplasms: results from the prospective longitudinal BoHemE study.Leukemia · 2026Article
- Genetic Determinants of Treatment-Related Bone Toxicity in Pediatric Acute Lymphoblastic Leukemia.Clinical pharmacology and therapeutics · 2026Article
- Iron overload induced by ferric derisomaltose and ferric carboxymaltose both increase FGF-23 levels and lead to osteomalacia and bone loss in normal mice.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Article
- Fibroblast growth factor 23 neutralizing antibody partially rescues bone loss and increases hematocrit in sickle cell disease mice.Scientific reports · 2025Article
- [Non-classical hormones from the fibroblast growth factor family].Problemy endokrinologii · 2024Review
- Increased Cadmium Load, Vitamin D Deficiency, and Elevated FGF23 Levels as Pathophysiological Factors Potentially Linked to the Onset of Acute Lymphoblastic Leukemia: A Review.Journal of personalized medicine · 2024Review
- Bone marrow transplantation reduces FGF-23 levels and restores bone formation in myelodysplastic neoplasms.Leukemia · 2024Article
- 1,25-Dihydroxyvitamin D3 regulates furin-mediated FGF23 cleavage.JCI insight · 2023Article
- A novel Hoxd13 mutation causes synpolydactyly and promotes osteoclast differentiation by regulating pSmad5/p65/c-Fos/Rank axis.Cell death & disease · 2023Article
- The link between bone-derived factors osteocalcin, fibroblast growth factor 23, sclerostin, lipocalin 2 and tumor bone metastasis.Frontiers in endocrinology · 2023Review
- The mesenchymal compartment in myelodysplastic syndrome: Its role in the pathogenesis of the disorder and its therapeutic targeting.Frontiers in oncology · 2023Review
- Exploration of the skeletal phenotype of theFrontiers in endocrinology · 2023Article
- Extracellular Vesicles in Myeloid Neoplasms.International journal of molecular sciences · 2022Review
- Interconnections of fibroblast growth factor 23 and klotho with erythropoietin and hypoxia-inducible factor.Molecular and cellular biochemistry · 2022Review
- Bone Marrow Niches and Tumour Cells: Lights and Shadows of a Mutual Relationship.Frontiers in immunology · 2022Review
- Bone marrow sinusoidal endothelium controls terminal erythroid differentiation and reticulocyte maturation.Nature communications · 2021Article
- Nature or Nurture? Role of the Bone Marrow Microenvironment in the Genesis and Maintenance of Myelodysplastic Syndromes.Cancers · 2021Review
- The HIF-PHI BAY 85-3934 (Molidustat) Improves Anemia and Is Associated With Reduced Levels of Circulating FGF23 in a CKD Mouse Model.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- Hypoxia Pathway Proteins are Master Regulators of Erythropoiesis.International journal of molecular sciences · 2020Review
- Role of Fibroblast Growth Factor 23 (FGF23) and αKlotho in Cancer.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myelodysplastic syndromes (MDS) are clonal malignant hematopoietic disorders in the elderly characterized by ineffective hematopoiesis. This is accompanied by an altered bone microenvironment, which contributes to MDS progression and higher bone fragility. The underlying mechanisms remain largely unexplored. Here, we show that myelodysplastic NUP98‑HOXD13 (NHD13) transgenic mice display an abnormally high number of osteoblasts, yet a higher fraction of nonmineralized bone, indicating delayed bone mineralization. This was accompanied by high fibroblast growth factor-23 (FGF-23) serum levels, a phosphaturic hormone that inhibits bone mineralization and erythropoiesis. While Fgf23 mRNA expression was low in bone, brain, and kidney of NHD13 mice, its expression was increased in erythroid precursors. Coculturing these precursors with WT osteoblasts induced osteoblast marker gene expression, which was inhibited by blocking FGF-23. Finally, antibody-based neutralization of FGF-23 in myelodysplastic NHD13 mice improved bone mineralization and bone microarchitecture, and it ameliorated anemia. Importantly, higher serum levels of FGF‑23 and an elevated amount of nonmineralized bone in patients with MDS validated the findings. C‑terminal FGF‑23 correlated negatively with hemoglobin levels and positively with the amount of nonmineralized bone. Thus, our study identifies FGF-23 as a link between altered bone structure and ineffective erythropoiesis in MDS with the prospects of a targeted therapeutic intervention.
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