Research trends of mitochondrial dysfunction in hepatic fibrosis: a bibliometric analysis

Xingtao Jin^1,2Yanlu Ma^1,2Yiqiang Tang^1,2Fengjie Qiao^1,2Tong Xiao^1,2Yu Cui^1,2Man Li^2,3*Yueqiu Gao^2,3*

• ¹Institute of Cellular Immunity Laboratory, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China
• ²Institute of Shanghai Key Laboratory of Traditional Chinese Clinical Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China
• ³Institute of Infectious Diseases, Shanghai Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China

Background: Hepatic fibrosis is a progressive pathological process driven by multiple chronic liver injury factors. Increasing evidence highlights that mitochondrial dysfunction serves as a pivotal mechanism in the onset and progression of hepatic fibrosis. Methods: A systematic search of the Web of Science Core Collection (WoSCC) and Scopus databases identified 1,634 relevant articles published between January 2005 and December 2025. Following the PRISMA guidelines, duplicate removal and quality control were performed. Bibliometric analysis tools including VOSviewer, CiteSpace, and Scimago Graphica were utilized to extract or calculate evaluation metrics, enabling analysis and visualization of knowledge maps. Publications were categorized by country, institution, author, journal, highly cited papers, and keywords. These variables were compared in terms of publication output and academic impact, including metrics such as citation counts, citation impact, H-index, and journal impact factor. Results: A total of 1,634 relevant publications were retrieved, originating from 92 countries or regions and 2858 research institutions. China and the United States led in both publication volume and impact; the most prolific institution was the Centro de Investigación Biomédica en Red (CIBER), followed by the University of California System. The International Journal of Molecular Sciences was the most frequently publishing journal, while Hepatology was the most highly cited journal. Heidari, Reza was the most prolific author; the five most cutting-edge keywords identified were oxidative stress, apoptosis, mitophagy, hepatic stellate cells, and reactive oxygen species. We confirmed three major research hotspots: activation of hepatic stellate cells, imbalance in mitochondrial quality control, and the vicious cycle of oxidative stress. Conclusions: Based on our previous discussions, mitochondria are increasingly recognized as central to the onset and progression of hepatic fibrosis. Related research is advancing rapidly and has become a key area for interdisciplinary collaboration. Future efforts should focus on: validating mitochondrial function biomarkers such as circulating mtDNA and mitochondria-specific metabolites; refining patient stratification based on mitochondrial dysfunction phenotypes (such as metabolic imbalance type, oxidative stress type); and advancing therapeutic strategies targeting mitochondrial quality control, metabolism, and redox balance. This will translate deep mechanistic insights into effective solutions for improving the clinical management of hepatic fibrosis.