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Background <p>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.</p> Methods <p>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.</p> Results <p>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.</p> Conclusions <p>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.</p>

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Global research trends on the associations between chronic kidney disease and mitochondria: insights from the bibliometric analysis

  • 期刊论文

  • 发表日期：

    2025年2月28日

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  • Xinfang Tang,
  • Anna Zhang,
  • Xiaojuan Feng,
  • Wenjuan Wang,
  • Fanghong Chen,
  • Yijie Tao,
  • Chuyan Wu,
  • Feng Jiang

摘要

Background

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.

Methods

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.

Results

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.

Conclusions

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.