Curr Med Chem. 2026 Mar 11. doi: 10.2174/0109298673417791251204121930. Online ahead of print.
ABSTRACT
BACKGROUND: Growing evidence implicates mitochondrial dysfunction as a pivotal contributor to glaucoma pathogenesis through oxidative stress, autophagy, and apoptotic pathways. However, systematic analyses of research collaboration patterns, key themes, and emerging trends in this field remain limited.
METHODS: We retrieved relevant publications from the Web of Science (WOS) database (1999-2024) for bibliometric analysis. Visualization was generated using VOSviewer and CiteSpace, with complementary analysis in Charticulator and Excel. Journal impact factors from WOS were used to assess publication influence.
RESULTS: This study analyzed 397 publications and found a fluctuating annual increase in both publications and citations in this research area. The United States emerged as the most productive nation in terms of publication volume. Investigative Ophthalmology & Visual Science was identified as the predominant journal in this field. Among individual researchers, Dr. Kim Keun Young was distinguished as a leading contributor. The most frequently occurring terms were: glaucoma, mitochondria, Oxidative Stress (OS), apoptosis, and Ischemia-Reperfusion Injury (IRI). Notably, the mitochondrial inhibitors were identified as promising therapeutic candidates for ophthalmic disorders. Our findings demonstrated the therapeutic potential of mitochondria through metabolic modulation and neuroprotective mechanisms, while identifying oxidative stress, autophagy dysregulation, and apoptotic pathways as critical pathological mediators. The analysis offered valuable insights for developing mitochondria-targeted therapies.
DISCUSSION: This comprehensive bibliometric analysis reveals a steady growth in research focusing on mitochondrial dysfunction in glaucoma, with the United States leading in scholarly output. The identified trends underscore a critical shift: emerging cellular and molecular insights are actively guiding the development of targeted and personalized therapeutic strategies for glaucoma. We acknowledge that our study has limitations inherent to bibliometric methodology. The literature search was restricted to articles and reviews within the Web of Science Core Collection. However, the exclusion of other major databases and clinical publication types may create a bias, overrepresenting basic research and underrepresenting clinical findings. Additionally, variations in the analytical algorithms of tools such as VOSviewer and CiteSpace may influence the resultant data patterns. Despite these limitations, the study offers a systematic mapping of the research landscape and provides a clear guide for future research directions in this field.
CONCLUSION: This study provided a comprehensive analysis of scientific advancements in this field, highlighting the pivotal role of mitochondrial dysfunction in glaucoma pathogenesis and proposing strategic directions for developing novel therapeutic approaches in ophthalmic disorders.
PMID:41837485 | DOI:10.2174/0109298673417791251204121930