ReviewEFORT open reviews2024
Mitochondrial maintenance as a novel target for treating steroid-induced osteonecrosis of femoral head: a narrative review.
Review in EFORT open reviews, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed.
- Mitochondrial Communication Networks in the Bone Microenvironment: From the Maintenance of Homeostasis to Translational Interventions for Bone Diseases.Stem cell reviews and reports · 2026Review
- From Physicochemical Properties to Rehabilitation Outcomes: Understanding Corticosteroid Injection Adverse Effects.International journal of molecular sciences · 2026Review
- Identifying coagulation-related biomarkers in steroid-induced osteonecrosis of the femoral head: implications for early diagnosis and treatment.Clinical and experimental medicine · 2026Article
- Regulating Glucose Metabolism Enzymes for Osteoporosis Therapy: Current and Future Approaches.International journal of molecular sciences · 2026Review
- DMOG pretreatment restores osteogenic-adipogenic balance and mitochondrial function in ONFH BMSCs through the HIF-1α/Homer3 pathway.Stem cell research & therapy · 2026Article
- Ascorbic Acid Modulates Collagen Properties in Glucocorticoid-Induced Osteoporotic Bone: Insights into Chemical, Mechanical, and Biological Regulation.Advanced healthcare materials · 2026Article
- Kaempferol Alleviates Glucocorticoid-Induced Osteonecrosis of the Femoral Head by Modulating Macrophage M1/M2 Polarization Through RhoA/ROCK-Mediated Mitophagy Activation.Biomedicines · 2026Article
- Complementary roles of HMGB1 and PRDX4 in the pathophysiology of steroid-associated osteonecrosis of the femoral head: a histopathological and immunohistochemistry study.Virchows Archiv : an international journal of pathology · 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
- Before taurine is recommended for stroke-like epsiodes in m.3243A>G carriers, its efficacy must be demonstrated by appropriate studies.CEN case reports · 2025Article
- Update on the correlation between mitochondrial function and osteonecrosis of the femoral head osteocytes.Redox report : communications in free radical research · 2025Review
- Immunomodulatory Mechanisms of Rehmanniae Radix Praeparata-Achyranthes Root-Chinese Angelica Root Combination in Nontraumatic Osteonecrosis of the Femoral Head: A Comprehensive Network Pharmacology and Molecular Docking Study Focusing on Immunological Pathways.Mediators of inflammation · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of steroid-induced osteonecrosis of the femoral head (SONFH) remains unclear; however, emerging evidence suggests that mitochondrial injury plays a significant role. This review aims to elucidate the involvement of mitochondrial dysfunction in SONFH and explore potential therapeutic targets. A comprehensive literature search was conducted in PubMed, Web of Science, and Elsevier ScienceDirect, focusing on mitochondrial homeostasis, including mitophagy, mitochondrial biogenesis, mitochondrial dynamics, and oxidative stress in SONFH. Ultimately, we included and analyzed a total of 16 studies. Glucocorticoids initially promote but later inhibit mitochondrial biogenesis in osteoblasts, leading to excessive ROS production and mitochondrial dysfunction. This dysfunction impairs osteoblast survival and bone formation, contributing to SONFH progression. Key proteins such as mitochondrial transcription factor A (TFAM) and peroxisome proliferator-activated receptor γ coactivator 1-α (PGC1α) are potential therapeutic targets for promoting mitochondrial biogenesis and reducing ROS-induced damage. Enhancing mitochondrial function and reducing oxidative stress in osteoblasts may prevent or slow the progression of SONFH. Future research should focus on developing these strategies.
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Registered trials
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