ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020
Erythropoietin signaling in osteoblasts is required for normal bone formation and for bone loss during erythropoietin-stimulated erythropoiesis.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Osteocyte-derived erythroferrone regulates liver hepcidin during stress erythropoiesis.Blood advances · 2026Article
- Erythropoietin and bone health: Single high-dose administration triggers bone loss in mice.Bone reports · 2026Article
- Duration, dose, and responsiveness to erythropoiesis-stimulating agents and risk of osteoporotic fracture among patients with chronic kidney disease in Hong Kong: a nested case-control study.EClinicalMedicine · 2025Article
- Breaking the noninflamed barrier: tumor-secreted erythropoietin as a master regulator of immunosuppressive macrophages.Journal of the National Cancer Center · 2025Article
- Erythropoietin delivery through kidney organoids engineered with an episomal DNA vector.Stem cell research & therapy · 2025Article
- The mediating role of BMI in the relationship between OSAHS and bone metabolism in male patients with T2DM.Sleep & breathing = Schlaf & Atmung · 2025Article
- Pharmacological inhibition of HIF2 protects against bone loss in an experimental model of estrogen deficiency.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- In-silico analysis predicts disruption of normal angiogenesis as a causative factor in osteoporosis pathogenesis.BMC genomic data · 2024Article
- Erythropoietin regulates osteoclast formation via up-regulating PPARγ expression.Molecular medicine (Cambridge, Mass.) · 2024Article
- Transforming the Niche: The Emerging Role of Extracellular Vesicles in Acute Myeloid Leukaemia Progression.International journal of molecular sciences · 2024Review
- Erythropoietin and Skeletal Cells CrossTalks in Physiology and Disease.Current opinion in endocrine and metabolic research · 2023Article
- Local YB-1, Epo, and EpoR concentrations in fractured bones: results from a porcine model of multiple trauma.European journal of medical research · 2023Article
- Erythropoietin Receptor (EPOR) Signaling in the Osteoclast Lineage Contributes to EPO-Induced Bone Loss in Mice.International journal of molecular sciences · 2022Article
- Hypoxia-Inducible Factors Signaling in Osteogenesis and Skeletal Repair.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
- A New Target of Dental Pulp-Derived Stem Cell-Based Therapy on Recipient Bone Marrow Niche in Systemic Lupus Erythematosus.International journal of molecular sciences · 2022Review
- Epo/EpoR signaling in osteoprogenitor cells is essential for bone homeostasis and Epo-induced bone loss.Bone research · 2021Article
- Review
- STAT5 as a Key Protein of Erythropoietin Signalization.International journal of molecular sciences · 2021Review
- Erythropoietin treatment and the risk of hip fractures in hemodialysis patients.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Erythropoietin (EPO) regulates erythropoiesis by binding to erythropoietin receptor (Epor) on erythroid progenitor cells. Epor is also expressed on bone forming osteoblasts and bone loss accompanies EPO-stimulated erythropoiesis in mice. Mice with Epor restricted to erythroid tissue exhibit reduced bone and increased marrow adipocytes; in contrast, transgenic mice (Tg) with osteoblastic-specific deletion of Epor exhibit reduced trabecular bone with age without change in marrow adipocytes. By 12 weeks, male Tg mice had 22.2% and female Tg mice had 29.6% reduced trabecular bone volume (BV) compared to controls. EPO administration (1200 U/kg) for 10 days reduced trabecular bone in control mice but not in Tg mice. There were no differences in numbers of osteoblasts, osteoclasts, and marrow adipocytes in Tg mice, suggesting independence of EPO signaling in mature osteoblasts, osteoclasts, and adipocytes. Female Tg mice had increased number of dying osteocytes and male Tg mice had a trend for more empty lacunae. Osteogenic cultures from Tg mice had reduced differentiation and mineralization with reduced Alpl and Runx2 transcripts. In conclusion, endogenous EPO-Epor signaling in osteoblasts is important in bone remodeling, particularly trabecular bone and endogenous Epor expression in osteoblasts is required for bone loss accompanying EPO-stimulated erythropoiesis.
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Registered trials
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