ArticleEndocrine journal2025
Knockdown of Gfi1 increases BMSCs exosomal miR-150-3p to inhibit osteoblast ferroptosis in steroid-induced osteonecrosis of the femoral head through BTRC/Nrf2 axis.
Article in Endocrine journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The role of ferroptosis in osteoporosis: a cellular perspective on osteoblast, osteoclast and osteocyte dysfunction.Frontiers in endocrinology · 2026Pooled it
- The miR-212-3p/transferrin axis promotes bone regeneration by modulating iron homeostasis through Schwann cell Exosome-BMSCs communication.Bioactive materials · 2026Article
- Recent advances in glucocorticoid regulation of bone and the bone marrow niche: Genetic and pharmacological approaches to understand and prevent bone loss.Current opinion in endocrine and metabolic research · 2026Article
- Progress of Programmed Cell Death in Steroid-Induced Osteonecrosis of the Femoral Head.Orthopaedic surgery · 2026Review
- Mesenchymal stem cell-derived extracellular vesicles for disease therapy by regulating ferroptosis: focus on diabetes mellitus and diabetic complications.Stem cell research & therapy · 2025Review
- Targeting ferroptosis to rescue osteogenic differentiation in BRONJ-affected jawbone mesenchymal stem cells: the role of miR-145-3p and exosome-mediated therapy.Journal of nanobiotechnology · 2025Article
- Growth factor independence 1 ameliorates osteoarthritis by inhibiting chondrocyte ferroptosis via inactivation of MAPK signaling pathway.Journal of orthopaedic translation · 2025Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ferroptosis of osteoblasts has been demonstrated to play a significant role in the development of steroid-induced osteonecrosis of the femoral head (SONFH). Additionally, microRNAs (miRNAs) have been identified as regulators of SONFH progression. However, the precise role of miRNAs in the regulation of osteoblast ferroptosis remains unclear. This study explored the role of exosomal miR-150-3p, derived from bone marrow mesenchymal stem cells (BMSCs), in osteoblast ferroptosis in SONFH. Dexamethasone (DEX) was used to treat osteoblasts to induce ferroptosis. BMSCs exosomes with different levels of miR-150-3p were introduced into a co-culture with the cells. To verify the targeting relationship between growth factor independence 1 (Gfi1) and the miR-150-3p promoter, as well as between miR-150-3p and beta-transducin repeat containing E3 ubiquitin protein ligase (BTRC), respectively, chromatin immunoprecipitation (ChIP), RNA immunoprecipitation (RIP), and dual luciferase assays were employed. It was found that BMSCs-Exos-miR-150-3p mitigated DEX-triggered ferroptosis in osteoblasts. MiR-150-3p directly targeted BTRC, leading to its downregulation in osteoblasts. The BTRC/Nuclear factor erythroid 2-related factor 2 (Nrf2) pathway was involved in the inhibition of DEX-induced osteoblast ferroptosis by BMSCs-Exos-miR-150-3p. Overexpression of BTRC reversed the inhibitory effect of BMSCs-Exos-miR-150-3p. In a SONFH rat model, BMSCs-Exos-miR-150-3p alleviated ferroptosis in osteoblasts through BTRC/Nrf2. In addition, Gfi1 bonded to the miR-150-3p promoter and inhibited its transcription. Gfi1 silencing elevated miR-150-3p levels and improves cell viability of BMSCs. In conclusion, our results suggest that BMSCs-Exos-miR-150-3p alleviates SONFH by suppressing ferroptosis through the regulation of BTRC/Nrf2 and miR-150-3p may be a potential target for SONFH treatment.
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