SYSTEMATIC REVIEW article
Front. Med.
Sec. Pathology
Volume 12 - 2025 | doi: 10.3389/fmed.2025.1597116
Advances in research on the relationship between mitochondrial dysfunction and osteoporosis: a bibliometric study from 2014 to 2024
Provisionally accepted
- 1Changchun University of Chinese Medicine, Changchun, Jilin Province, China
- 2The Affiliated Hospital of Changchun University of Traditional Chinese Medicine, Changchun, Jilin Province, China
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Osteoporosis, characterized by reduced bone mineral density and increased risk of fracture, poses a major health challenge, especially in an aging population. Mitochondria play a crucial role in cellular energy production and homeostasis. Recent evidence indicates that mitochondrial dysfunction is closely related to the pathogenesis of osteoporosis.This study conducted a comprehensive bibliometric analysis to explore the relationship between mitochondrial dysfunction and osteoporosis (OP), utilizing data from the Web of Science Core Collection (WoSCC) spanning 2014-2024. A total of 780 articles were analyzed using CiteSpace and VOSviewer to visualize research trends, collaboration networks, and emerging hotspots. The annual publication output demonstrated a significant upward trajectory, with China and the United States leading contributions. Key journals such as Journal of Biological Chemistry and Nature were identified as authoritative sources, while oxidative stress (177 occurrences), apoptosis, mitophagy, and mitochondrial transfer emerged as core research themes. CiteSpace cluster analysis revealed emerging frontiers, including ferroptosis and SIRT1 signaling pathways, which exhibited rapid growth in keyword frequency and citation bursts. VOSviewer mapping highlighted interdisciplinary linkages between mitochondrial quality control, redox balance, and bone metabolism. Clinical implications were underscored by therapeutic strategies targeting oxidative stress, such as SIRT1 activators, vitamin K2, and nanoparticle-based interventions, which showed promise in preclinical models for restoring bone homeostasis.Additionally, mitochondrial transfer mechanisms and ferroptosis inhibitors were proposed as novel approaches for bone defect repair and diabetic osteoporosis management. These findings provide new insights into the molecular mechanisms of osteoporosis and potential targets for future prevention and treatment strategies. Overall, this study promotes our understanding of the complex interactions between mitochondrial function and bone health, and provides a valuable direction for further research.
Keywords: mitochondria1, osteoporosis2, Oxidative Stress3, bone homeostasis4, mitochondrial metabolism5
Received: 20 Mar 2025; Accepted: 03 Jun 2025.
Copyright: © 2025 Zhang, YU, Han, Si, LI and Han. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Jicheng Han, The Affiliated Hospital of Changchun University of Traditional Chinese Medicine, Changchun, 130021, Jilin Province, China
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