线粒体功能障碍与骨质疏松症关系的研究进展:一项2014年至2024年的文献计量学研究
Advances in research on the relationship between mitochondrial dysfunction and osteoporosis: a bibliometric study from 2014 to 2024.
作者信息
Zhang Yun-Song, Yu Jia-Nan, Han Ming-Ze, Si Bin, Li Zhen-Hua, Han Ji-Cheng
机构信息
School of Integrated Traditional Chinese and Western Medicine, Changchun University of Chinese Medicine, Changchun, China.
School of Traditional Chinese Medicine, Changchun University of Chinese Medicine, Changchun, China.
出版信息
Front Med (Lausanne). 2025 Jul 3;12:1597116. doi: 10.3389/fmed.2025.1597116. eCollection 2025.
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.
引言
骨质疏松症以骨矿物质密度降低和骨折风险增加为特征,对老年人群构成了重大的健康挑战。新出现的证据表明,线粒体功能障碍在其发病机制中起关键作用,不过目前缺乏对研究趋势和治疗潜力的全面分析。
方法
我们使用CiteSpace和VOSviewer对来自科学网核心合集(2014 - 2024年)的780篇文章进行了文献计量分析,以可视化研究趋势、合作网络和新兴热点。
结果
年度出版物呈显著上升趋势,中国和美国是主要贡献者。确定了关键期刊(如《生物化学杂志》《自然》)和核心主题:氧化应激(出现177次)、细胞凋亡、线粒体自噬和线粒体转移。聚类分析揭示了新兴前沿领域,包括铁死亡和SIRT1信号通路,其引用增长迅速。跨学科联系突出了线粒体质量控制、氧化还原平衡和骨代谢之间的关联。
讨论
针对氧化应激的治疗策略(如SIRT1激活剂、维生素K2、基于纳米颗粒的干预措施)在恢复骨稳态方面显示出临床前前景。线粒体转移机制和铁死亡抑制剂被提议作为骨缺损修复和糖尿病性骨质疏松症管理的新方法。本研究为骨质疏松症的预防和治疗提供了新的分子见解和未来方向。