ArticleBMC musculoskeletal disorders2023
Erythropoietin suppresses osteoblast apoptosis and ameliorates steroid-induced necrosis of the femoral head in rats by inhibition of STAT1-caspase 3 signaling pathway.
Article in BMC musculoskeletal disorders, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 4 citations in OpenAlex.
- Erythropoietin and bone health: Single high-dose administration triggers bone loss in mice.Bone reports · 2026Article
- Erythropoietin in tissue engineering and beyond: a multifunctional macromolecule with emerging roles in organoids, immune modulation, and cancer research.Frontiers in bioengineering and biotechnology · 2026Review
- Research Progress of Multiple Molecular Signal Pathways in the Pathogenesis of Steroid-induced Osteonecrosis of the Femoral Head.Orthopedic reviews · 2026Article
- YTHDF3-associated m6A regulation and cuproptosis-related gene expression in steroid-induced osteonecrosis of the femoral head.Journal of molecular histology · 2025Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSteroid-induced avascular necrosis of the femoral head (SANFH) is characterized by osteoblast apoptosis, leading to a loss of bone structure and impaired hip joint function. It has been demonstrated that erythropoietin (EPO) performs a number of biological roles.
objectiveWe examined the effects of EPO on SANFH and its regulation of the STAT1-caspase 3 signaling pathway.
methodIn vitro, osteoblasts were treated with dexamethasone (Dex) or EPO. We identified the cytotoxicity of EPO by CCK-8, the protein expression of P-STAT1, cleaved-caspase9, cleaved-caspase3, Bcl-2, BAX, and cytochrome c by Western blotting, and evaluated the apoptosis of osteoblasts by flow cytometry. In vivo, we analyzed the protective effect of EPO against SANFH by hematoxylin and eosin (H&E), Immunohistochemical staining, and Micro-computed tomography (CT).
resultsIn vitro, EPO had no apparent toxic effect on osteoblasts. In Dex-stimulated cells, EPO therapy lowered the protein expression of BAX, cytochrome c, p-STAT1, cleaved-caspase9, and cleaved-caspase3 while increasing the expression of Bcl-2. EPO can alleviate the apoptosis induced by Dex. In vivo, EPO can lower the percentage of empty bone lacunae in SANFH rats.
conclusionThe present study shows that EPO conferred beneficial effects in rats with SANFH by inhibiting STAT1-caspase 3 signaling, suggesting that EPO may be developed as a treatment for SANFH.
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