ArticleThe Journal of biological chemistry2011
Glucocorticoids and tumor necrosis factor α increase oxidative stress and suppress Wnt protein signaling in osteoblasts.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.
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Who cites it
137 citing papers in PubMed, 273 citations in OpenAlex.
- Research efficacy of gaseous ozone therapy as an adjuvant to periodontal treatment on oxidative stress mediators in patients with type 2 diabetes: a randomized clinical trial.BMC oral health · 2023Trial
- Comparison of the effect of 18-month daily teriparatide administration on patients with rheumatoid arthritis and postmenopausal osteoporosis patients.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2014Trial
- Screening of a quinonoid compounds library identifies decylubiquinone as an antioxidant and anti-apoptotic agent against glucocorticoid-induced osteoporosis via CD39/CD73/adenosine axis.Bioactive materials · 2026Article
- Angiotensin converting enzyme-2 activation mitigates glucocorticoids-induced osteoporosis in rats by modulating oxidative stress, inflammation and the RANKL/OPG pathway.Pflugers Archiv : European journal of physiology · 2026Article
- TIGAR promotes osteogenic differentiation and ameliorates glucocorticoid-induced osteoporosis via autophagy-Nrf2-ROS axis.Genes & diseases · 2026Article
- The influence of hormonal changes during pregnancy on bone metabolism - a mini review.Frontiers in endocrinology · 2026Review
- Heart Failure but Not Myocardial Infarction Is Causing Bone Loss in Rodent Models in an FGF23-Independent Manner.International journal of molecular sciences · 2025Article
- Ceria nanoparticles guard against glucocorticoid induced bone homeostasis imbalance through the promotion of osteogenesis and inhibition of osteoclastogenesis.Materials today. Bio · 2025Article
- The role of bone in whole-body energy metabolism.Nature reviews. Endocrinology · 2025Review
- Update on the correlation between mitochondrial function and osteonecrosis of the femoral head osteocytes.Redox report : communications in free radical research · 2025Review
- New Perspectives on Postmenopausal Osteoporosis: Mechanisms and Potential Therapeutic Strategies of Sirtuins and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2025Review
- Article
- Isovitexin targets SIRT3 to prevent steroid-induced osteonecrosis of the femoral head by modulating mitophagy-mediated ferroptosis.Bone research · 2025Article
- Age-related inflammatory biomarkers in early-onset osteoporosis in females with Gaucher disease.Frontiers in endocrinology · 2025Article
- Mitochondrial maintenance as a novel target for treating steroid-induced osteonecrosis of femoral head: a narrative review.EFORT open reviews · 2024Review
- Global Trends in Research of Programmed Cell Death in Osteoporosis: A Bibliometric and Visualized Analysis (2000-2023).Orthopaedic surgery · 2024Review
- Protein kinase G2 activation restores Wnt signaling and bone mass in glucocorticoid-induced osteoporosis in mice.JCI insight · 2024Article
- Current Aspects of Selected Factors to Modulate Brain Health and Sports Performance in Athletes.Nutrients · 2024Review
- High-molecular-weight Hyaluronan Administration Inhibits Bone Resorption and Promotes Bone Formation in Young-age Osteoporosis Rats.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2024Article
- Relationship between Femoral Proximal Bone Quality Assessment by MRI IDEAL-IQ Sequence and Body Mass Index in Elderly Men.Tomography (Ann Arbor, Mich.) · 2024Article
77 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Endogenous glucocorticoids (GCs) and inflammatory cytokines contribute to the age-associated loss of bone mass and strength, but the molecular mechanisms responsible for their deleterious effects on the aging skeleton are unclear. Based on evidence that oxidative stress is a causal mechanism of the insulin resistance produced by either one of these two agents, we tested the hypothesis that their adverse skeletal effects also result from increased oxidative stress. We report that administration of prednisolone to mice increased reactive oxygen species (ROS) and the phosphorylation of p66(shc) (an amplifier of H(2)O(2) generation in mitochondria) in bone. Dexamethasone (Dex) and TNFα had a similar effect on osteoblastic cells in vitro. The generation of ROS by Dex and TNFα required PKCβ/p66(shc) signaling and was responsible for the activation of JNK and induction of apoptosis by both agents. The activity of Forkhead box O (FoxO) transcription factors was also increased in response to ROS; however, FoxO activation opposed apoptosis induced by Dex and TNFα. In addition, both agents suppressed Akt phosphorylation as well as Wnt-induced proliferation and osteoblast differentiation. However, the inhibitory actions on Wnt signaling were independent of PKCβ/p66(shc). Instead, they were mediated by inhibition of Akt and stimulation of FoxOs. These results demonstrate that ROS-induced activation of a PKCβ/p66(shc)/JNK signaling cascade is responsible for the pro-apoptotic effects of Dex and TNFα on osteoblastic cells. Moreover, modulation of Akt and FoxOs by GCs and TNFα are cell-autonomous mechanisms of Wnt/β-catenin antagonism contributing to the adverse effects of GC excess and inflammatory cytokines on bone alike.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.