ArticleMolecular medicine reports2018
Low-dose dexamethasone affects osteoblast viability by inducing autophagy via intracellular ROS.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 57 citations in OpenAlex.
- Regulating Glucose Metabolism Enzymes for Osteoporosis Therapy: Current and Future Approaches.International journal of molecular sciences · 2026Review
- Autophagy: regulating the seesaw of bone-fat balance.Frontiers in cell and developmental biology · 2025Review
- Asperuloside alleviates osteoporosis by promoting autophagy and regulating Nrf2 activation.Journal of orthopaedic surgery and research · 2024Article
- Targeting the mTOR-Autophagy Axis: Unveiling Therapeutic Potentials in Osteoporosis.Biomolecules · 2024Review
- Exercise-activated hepatic autophagy combined with silymarin is associated with suppression of apoptosis in rats subjected to dexamethasone induced- fatty liver damage.Molecular biology reports · 2024Article
- Dexamethasone Induced Osteocyte Apoptosis in Steroid-Induced Femoral Head Osteonecrosis through ROS-Mediated Oxidative Stress.Orthopaedic surgery · 2024Article
- Insights and implications of sexual dimorphism in osteoporosis.Bone research · 2024Review
- Metabolic bone disorders and the promise of marine osteoactive compounds.Cellular and molecular life sciences : CMLS · 2023Review
- Low-dose dexamethasone promotes osteoblast viability by activating autophagy via the SGK1/FOXO3a signaling pathway.Cell biology international · 2023Article
- Update on the Role of Glucocorticoid Signaling in Osteoblasts and Bone Marrow Adipocytes During Aging.Current osteoporosis reports · 2023Review
- Dexamethasone-Induced Fatty Acid Oxidation and Autophagy/Mitophagy Are Essential for T-ALL Glucocorticoid Resistance.Cancers · 2023Article
- Article
- The Impacts of COVID-19 on Musculoskeletal Health.Current osteoporosis reports · 2022Review
- N,N-Dimethylformamide inhibits high glucose-induced osteoporosis via attenuating MAPK and NF-κB signalling.Bone & joint research · 2022Article
- Autophagy in Bone Remodeling: A Regulator of Oxidative Stress.Frontiers in endocrinology · 2022Review
- Network-Based Pharmacology and Bioinformatics Study on the Mechanism of Action of Gujiansan in the Treatment of Steroid-Induced Avascular Necrosis of the Femoral Head.BioMed research international · 2022Article
- Bad to the Bone: The Effects of Therapeutic Glucocorticoids on Osteoblasts and Osteocytes.Frontiers in endocrinology · 2022Review
- The Signalling Effects of Photobiomodulation on Osteoblast Proliferation, Maturation and Differentiation: A Review.Stem cell reviews and reports · 2021Review
- Coronaviruses construct an interconnection way with ERAD and autophagy.Future microbiology · 2021Review
- Paeoniflorin Attenuates Dexamethasone-Induced Apoptosis of Osteoblast Cells and Promotes Bone Formation via Regulating AKT/mTOR/Autophagy Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoids (GCs) are closely associated with the progression of GC‑induced osteoporosis (GIOP) by inhibiting osteoblast viability. However, endogenous GCs are important for bone development. In addition, previous studies have demonstrated that GCs could induce autophagy, a cytoprotective process that is protective against various stressors. In the present study, the aim is to explore whether osteoblasts exhibited dose‑dependent viability in the presence of GCs due to autophagy. hFOB 1.19 osteoblasts were treated with various doses of dexamethasone (DEX; 10‑8‑10‑4 M) for 0, 24, 48 and 72 h. The results revealed a biphasic effect of DEX on the viability of hFOB 1.19 cells; a high dose of DEX (≥10‑6 M) accelerated cell apoptosis, while a low dose of DEX (10‑8 M) increased cell viability. Furthermore, significantly increased autophagy was observed in the low dose DEX treatment group, as indicated by the expression of the autophagy‑associated proteins beclin 1 and microtubule‑associated protein light chain 3, and the detection of autophagosomes. Another finding was that DEX upregulated intracellular reactive oxygen species (ROS), which was decreased by the autophagy agonist rapamycin. The increase in autophagy and cell viability associated with low‑dose DEX (10‑8 M) was suppressed by the ROS scavenger catalase and the autophagy inhibitor 3‑methyladenine. In conclusion, the results revealed that GCs affected osteoblast viability in a dose‑dependent manner. A low dose of GCs increased osteoblast viability by inducing autophagy via intracellular ROS. The results indicate that autophagy may be a novel mechanism by which osteoblasts survive GC exposure and provide a potential therapeutic target for treating GIOP.
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