SynthesisFrontiers in medicine2025
Advances in research on the relationship between mitochondrial dysfunction and osteoporosis: a bibliometric study from 2014 to 2024.
Synthesis in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Exercise-Induced Regulation of Bone Remodeling via Mitophagy: A Review of Current Evidence.Biomolecules · 2026Review
- Identification and validation of NETs-associated biomarkers in osteoporosis with diabetes.Scientific reports · 2026Article
- Exosomal miR-484 from lung adenocarcinoma promotes osteoclastogenesis and osteolytic bone metastasis by targeting PECAM1.Discover oncology · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Osteoporosis, characterized by reduced bone mineral density and increased fracture risk, poses a major health challenge in aging populations. Emerging evidence indicates that mitochondrial dysfunction plays a crucial role in its pathogenesis, though a comprehensive analysis of research trends and therapeutic potential is lacking. Methods: We conducted a bibliometric analysis of 780 articles from the Web of Science Core Collection (2014-2024) using CiteSpace and VOSviewer to visualize research trends, collaboration networks, and emerging hotspots. Results: Annual publications showed a significant upward trend, with China and the United States as leading contributors. Key journals (e.g., Journal of Biological Chemistry, Nature) and core themes were identified: oxidative stress (177 occurrences), apoptosis, mitophagy, and mitochondrial transfer. Cluster analysis revealed emerging frontiers, including ferroptosis and SIRT1 signaling pathways, with rapid citation growth. Interdisciplinary linkages highlighted connections between mitochondrial quality control, redox balance, and bone metabolism. Discussion: Therapeutic strategies targeting oxidative stress (e.g., SIRT1 activators, vitamin K2, nanoparticle-based interventions) showed preclinical promise in restoring bone homeostasis. Mitochondrial transfer mechanisms and ferroptosis inhibitors were proposed as novel approaches for bone defect repair and diabetic osteoporosis management. This study provides new molecular insights and future directions for osteoporosis prevention and treatment.
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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.