ArticleInternational journal of molecular sciences2020
Erythropoietin Mediated Bone Loss in Mice Is Dose-Dependent and Mostly Irreversible.
Article in International journal of molecular sciences, 2020. 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, 13 citations in OpenAlex.
- Erythropoietin and bone health: Single high-dose administration triggers bone loss in mice.Bone reports · 2026Article
- Review
- Erythropoietin treatment and osteoporotic fracture risk in hemodialysis patients: A nationwide population-based study.Osteoporosis and sarcopenia · 2024Article
- Effects of Erythropoietin-Promoted Fracture Healing on Bone Turnover Markers in Cats.Journal of functional biomaterials · 2024Article
- Erythropoietin Receptor (EPOR) Signaling in the Osteoclast Lineage Contributes to EPO-Induced Bone Loss in Mice.International journal of molecular sciences · 2022Article
- Association Between Hemoglobin Levels and Osteoporosis in Chinese Patients with Type 2 Diabetes Mellitus: A Cross-Sectional Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Article
- Effect of Acetazolamide and Zoledronate on Simulated High Altitude-Induced Bone Loss.Frontiers in endocrinology · 2022Article
- The Non-Erythropoietic EPO Analogue Cibinetide Inhibits Osteoclastogenesis In Vitro and Increases Bone Mineral Density in Mice.International journal of molecular sciences · 2021Article
- Epo/EpoR signaling in osteoprogenitor cells is essential for bone homeostasis and Epo-induced bone loss.Bone research · 2021Article
- Intestinal-derived FGF15 protects against deleterious effects of vertical sleeve gastrectomy in mice.Nature communications · 2021Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
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Abstract
Recent studies have demonstrated that erythropoietin (EPO) treatment in mice results in trabecular bone loss. Here, we investigated the dose-response relationship between EPO, hemoglobin (Hgb) and bone loss and examined the reversibility of EPO-induced damage. Increasing doses of EPO over two weeks led to a dose-dependent increase in Hgb in young female mice, accompanied by a disproportionate decrease in trabecular bone mass measured by micro-CT (µCT). Namely, increasing EPO from 24 to 540 IU/week produced a modest 12% rise in Hgb (20.2 ± 1.3 mg/dL vs 22.7 ± 1.3 mg/dL), while trabecular bone volume fraction (BV/TV) in the distal femur decreased dramatically (27 ± 8.5% vs 53 ± 10.2% bone loss). To explore the long-term skeletal effects of EPO, we treated mice for two weeks (540 IU/week) and monitored bone mass changes after treatment cessation. Six weeks post-treatment, there was only a partial recovery of the trabecular microarchitecture in the femur and vertebra. EPO-induced bone loss is therefore dose-dependent and mostly irreversible at doses that offer only a minor advantage in the treatment of anemia. Because patients requiring EPO therapy are often prone to osteoporosis, our data advocate for using the lowest effective EPO dose for the shortest period of time to decrease thromboembolic complications and minimize the adverse skeletal outcome.
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Registered trials
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