ArticleApoptosis : an international journal on programmed cell death2023
Glucocorticoid-induced activation of NOX/ROS/NF-κB signaling in MSCs contributes to the development of GONFH.
Article in Apoptosis : an international journal on programmed cell death, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 16 citations in OpenAlex.
- Macrophage immunometabolic reprogramming in inflammatory repair failure in osteonecrosis of the femoral head.Journal of orthopaedic translation · 2026Review
- A bioactive magnesium alloy scaffold integrated with BMSCs-Loaded 3D microspheres synergistically promotes femoral head osteonecrosis repair by improving the osteogenic-angiogenic microenvironment.Bioactive materials · 2026Article
- Repeated photobiological regulation therapy alleviates inflammation in mice with experimental acute pancreatitis through ROS/NF-κB pathway.Lasers in medical science · 2026Article
- Advances in the mechanism for steroid-induced osteonecrosis of the femoral head.Bone research · 2026Review
- A Novel Murine Model to Study the Early Biological Events of Corticosteroid-Associated Osteonecrosis of the Femoral Head.Bioengineering (Basel, Switzerland) · 2026Article
- Cancer stem cell programs S-nitrosylation and deubiquitination of FoxP3 protein to promote regulatory T cell differentiation.Frontiers in immunology · 2026Article
- From pathogenesis to treatment: the role of autophagic cell death in GONFH and its potential mitigation by naringenin.Theranostics · 2026Article
- Computational and Experimental Biology Reveals Dihydroartemisinin's Efficacy Against Steroid-Induced Osteonecrosis of the Femoral Head Adjusting Ferroptosis via CCL17-PRDX6.Drug design, development and therapy · 2026Article
- New insights into the mechanism of microvascular rarefaction via endothelial-mesenchymal transition in steroid-induced osteonecrosis of femoral head.Scientific reports · 2025Article
- Hydroethanolic Extract ofPlants (Basel, Switzerland) · 2024Article
- Codonopsis pilosula polysaccharide suppresses the progression of non-small cell lung cancer by triggering NLRP3/GSDMD-dependent pyroptosis.Discover oncology · 2024Article
- Inhibition of insulin degrading enzyme suppresses osteoclast hyperactivity via enhancing Nrf2-dependent antioxidant response in glucocorticoid-induced osteonecrosis of the femoral head.Molecular medicine (Cambridge, Mass.) · 2024Article
- YTHDF2-Mediated m6A methylation inhibition by miR27a as a protective mechanism against hormonal osteonecrosis in BMSCs.BMC musculoskeletal disorders · 2024Article
- Pro-Inflammatory Signaling Cascade Markers, Oxidative Stress-Inflammatory Signaling Axis, and Chronic Total Occlusion of Tibial Artery in Elderly Patients Suffering from Occlusion of Coronary Arteries.Current topics in medicinal chemistry · 2024Article
- Metformin Modulates Cell Oxidative Stress to Mitigate Corticosteroid-Induced Suppression of Osteogenesis in a 3D Model.Journal of inflammation research · 2024Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study aimed to investigate the pathogenic factors of glucocorticoids (GCs)-induced osteonecrosis of the femoral head (GONFH) and its underlying pathogenesis in vivo and in vitro.
methodsRadiographical (µCT) scanning, histopathological, immunohistochemical, reactive oxygen species (ROS) and tunel staining were conducted on GONFH patients and rats. ROS, tunel, flow cytometry, alkaline phosphatase, Oil red O staining, reverse transcription‑quantitative PCR and western blotting were applied to elucidate the exact pathogenesis mechanism.
resultsClinical and animal studies demonstrated increased levels of ROS, aggravated oxidative stress (OS) microenvironment, augmented apoptosis and imbalance in osteogenic/lipogenic in the GONFH group compared to the control group. The fate of mesenchymal stem cells (MSCs) directed by GCs is a crucial factor in determining GONFH. In vitro studies further revealed that GCs promote excessive ROS production through the expression of NOX family proteins, leading to a deterioration of the OS microenvironment in MSCs, ultimately resulting in apoptosis and imbalance in osteogenic/lipogenic differentiation. Furthermore, our results confirmed that the NOX inhibitor-diphenyleneiodonium chloride and the NF-κB inhibitor-BAY 11-7082 ameliorated apoptosis and osteogenic/lipogenic differentiation imbalance of MSCs induced by an excess of GCs.
conclusionWe demonstrated for the first time that the aggravation of the OS microenvironment in MSCs caused by high doses of GCs leading to apoptosis and differentiation imbalance is a crucial factor in the pathogenesis of GONFH, mediated through activating the NOX/ROS/NF-κB signaling pathway.
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