Tang Xinfang, Zhang Anna, Feng Xiaojuan, Wang Wenjuan, Chen Fanghong, Tao Yijie, Wu Chuyan, Jiang Feng
Department of Nephrology, The Affiliated Lianyungang Municipal Oriental Hospital of Kangda College of Nanjing Medical University, Lianyungang Municipal Oriental Hospital, Lianyungang, China.
Department of Laboratory, The Affiliated Lianyungang Municipal Oriental Hospital of Kangda College of Nanjing Medical University, Lianyungang Municipal Oriental Hospital, Lianyungang, China.
Int Urol Nephrol. 2025 Feb 28. doi: 10.1007/s11255-025-04437-x.
Chronic kidney disease (CKD) is a global health burden characterized by a progressive and irreversible loss of kidney function. Mitochondrial dysfunction has emerged as a pivotal factor in CKD pathogenesis, contributing to renal cell injury, inflammation, and fibrosis through mechanisms such as oxidative stress and impaired bioenergetics. This study aimed to provide a comprehensive bibliometric analysis of global research trends on the associations between CKD and mitochondria over the past two decades.
A bibliometric analysis was conducted using the Web of Science Core Collection database, focusing on publications from 2004 to 2024. Data were analyzed using Citespace and VOSviewer to visualize publication trends, key contributors, keyword co-occurrences, and collaboration networks.
A total of 2,870 publications were identified, with a significant increase in annual output observed after 2010. The United States, China, and Japan were the leading contributors, fostering strong international collaborations. Institutional analysis highlighted the prominent roles of the US Department of Veterans Affairs and the University of California System. Key authors, such as Jose Pedraza-Chaverri and HM Kang, and influential studies addressing mitochondrial quality control and metabolic reprogramming were identified. Keyword analysis revealed major research themes, including oxidative stress, ischemia-reperfusion injury, and fatty acid oxidation, with recent trends emphasizing mitochondrial dynamics and autophagy.
This analysis underscored the growing recognition of mitochondrial dysfunction in CKD pathogenesis and highlighted the interdisciplinary nature of this field. The findings revealed key research trends, influential contributors, and emerging topics, providing a foundation for future studies and the development of targeted mitochondrial therapies. These insights hold promise for advancing the understanding and treatment of CKD through precision medicine approaches. Specifically, therapeutic strategies aimed at enhancing mitochondrial biogenesis, promoting mitophagy, and restoring metabolic balance may offer novel avenues for delaying CKD progression and mitigating renal dysfunction. Integrating these mitochondrial-targeted interventions into current clinical practice could improve patient outcomes and guide the development of more effective treatment protocols.
慢性肾脏病(CKD)是一种全球性的健康负担,其特征是肾功能进行性且不可逆地丧失。线粒体功能障碍已成为CKD发病机制中的关键因素,通过氧化应激和生物能量学受损等机制导致肾细胞损伤、炎症和纤维化。本研究旨在对过去二十年全球关于CKD与线粒体关联的研究趋势进行全面的文献计量分析。
使用Web of Science核心合集数据库进行文献计量分析,重点关注2004年至2024年的出版物。使用Citespace和VOSviewer分析数据,以可视化出版趋势、主要贡献者、关键词共现情况和合作网络。
共识别出2870篇出版物,2010年后年产出显著增加。美国、中国和日本是主要贡献者,促进了强大的国际合作。机构分析突出了美国退伍军人事务部和加利福尼亚大学系统的突出作用。确定了关键作者,如Jose Pedraza-Chaverri和HM Kang,以及涉及线粒体质量控制和代谢重编程的有影响力的研究。关键词分析揭示了主要研究主题,包括氧化应激、缺血再灌注损伤和脂肪酸氧化,近期趋势强调线粒体动力学和自噬。
该分析强调了对CKD发病机制中线粒体功能障碍的认识不断增加,并突出了该领域的跨学科性质。研究结果揭示了关键研究趋势、有影响力的贡献者和新兴主题,为未来研究和靶向线粒体治疗的发展提供了基础。这些见解有望通过精准医学方法推进对CKD的理解和治疗。具体而言,旨在增强线粒体生物合成、促进线粒体自噬和恢复代谢平衡的治疗策略可能为延缓CKD进展和减轻肾功能障碍提供新途径。将这些线粒体靶向干预措施纳入当前临床实践可改善患者预后,并指导制定更有效的治疗方案。