Global Research Progress of Mitochondria and Hypoxic-Ischemic Encephalopathy: A Comprehensive Bibliometric Analysis

Background Hypoxic-ischemic encephalopathy is a serious neurologic condition caused by reduced blood and oxygen supply to the brain, typically occurring during birth. Mitochondria play a crucial role in the pathophysiological mechanisms of hypoxic-ischemic encephalopathy, yet a comprehensive bibliometric analysis of this research area is lacking. This study aims to identify research hotspots and trends related to mitochondria and hypoxic-ischemic encephalopathy through a detailed bibliometric analysis. Methods We searched the Web of Science Core Collection for studies on hypoxic-ischemic encephalopathy and mitochondria published between 2004 and 2024. Using VOSviewer, Citespace, and the R package “bibliometrix,” we conducted a comprehensive analysis to explore research trends, key topics, and collaborations. Results A total of 162 eligible articles were identified. The annual number of publications has increased over time, with peaks in recent years. The top contributing countries were China, the United States, and the United Kingdom, showing extensive international collaborations. Major institutions include Augusta University, Southern Medical University, and the University of the Basque Country. The leading journals were the International Journal of Molecular Sciences and Neurobiology of Disease . Keyword analysis highlighted neuroprotection, apoptosis, oxidative stress, and ferroptosis as primary research themes. Influential references with strong citation bursts were identified, indicating their impact on the field. Conclusion This is the first bibliometric analysis of research on mitochondria and hypoxic-ischemic encephalopathy, highlighting key trends and hotspots. Our findings provide valuable insights into the development and direction of research in this field and emphasize the importance of mitochondria in understanding and potentially mitigating the impacts of hypoxic-ischemic encephalopathy.