ArticleToxicology research2023
Dexamethasone-induced mitochondrial ROS-mediated inhibition of AMPK activity facilitates osteoblast necroptosis.
Article in Toxicology research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- AMPK as a central regulator of necroptosis: mechanistic insights and therapeutic implications.Journal of physiology and biochemistry · 2026Review
- Redox-modulation of regulated cell death: implications for synergistic anticancer therapies.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Progress of Programmed Cell Death in Steroid-Induced Osteonecrosis of the Femoral Head.Orthopaedic surgery · 2026Review
- Different Forms of Regulated Cell Death in Type-2-Diabetes-Mellitus-Related Osteoporosis: A Focus on Mechanisms and Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Immunological mechanisms in steroid-induced osteonecrosis of the femoral head.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long-term or high-dose glucocorticoid use can lead to serious orthopedic complications, including femoral head necrosis. Both basic and clinical studies have shown that high doses dexamethasone (Dex) can directly induce osteoblasts death. This study investigated the mechanism underlying Dex induced osteoblast death. In this study, we showed that Dex induces osteoblast necroptosis, rather than apoptosis, through the inhibition of AMP-activated protein kinase (AMPK) activity. We also demonstrated that inactivation of AMPK-mediated necroptosis is through receptor-interacting protein kinase 3 (RIP3), but not RIP1. Furthermore, we found that Dex-induced necroptosis is dependent on mitochondrial reactive oxygen species (ROS) following with directly activation of RIP1 and inactivation of AMPK. These findings provide new insights into the mechanism of Dex-induced osteoblast death and may have implications for the development of new therapies for osteoporosis and other bone-related diseases.
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Registered trials
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