Global Research Trends in Oxidative Stress and Myocardial Fibrosis: A Dual-Software Bibliometric Study.

Objective: To conduct a visualization analysis of the literature on the role of oxidative stress in myocardial fibrosis (MF), explore the research progress, frontier hotspots, and development trends in this field, with the aim of providing a reference for the research on the prevention and treatment of MF related to oxidative stress.

Methods: Web of Science was selected as the data source, and the relevant English literature on the role of oxidative stress in MF from the database establishment to December 31, 2024 was collected. Bibliometric methods were used for statistical analysis of the literature that met the research standards, and CiteSpace 6.3.R2 and VOSviewer 1.6.20 software were used for visualization of information such as publishing countries, institutions, authors, and keywords.

Results: A total of 1831 SCI articles were included. The global publication volume showed an upward trend year by year, Publications increased by 16% annually after 2014, with China and the United States leading in publication volume. Keyword and cited literature analysis showed that the research hotspots and frontiers in this field mainly include the phenomenon of extracellular matrix (ECM) cell migration, the activation of the renin-angiotensin-aldosterone system, the regulatory mechanisms of oxidative stress in MF of different etiologies, and the mechanisms of action of oxidative stress in MF.

Conclusion: The field of research into the role of oxidative stress in myocardial fibrosis is currently experiencing a period of rapid expansion. By leveraging the complementary strengths of CiteSpace for analyzing temporal and geographic trends, and VOSviewer for mapping collaboration networks, researchers have gained multidimensional insights into this area. The identification of the NLRP3 inflammasome as the fastest-growing research frontier, highlights its potential as a novel therapeutic target for clinical investigation. The mechanism by which oxidative stress activates the NLRP3 inflammasome signaling pathway to promote myocardial fibrosis is likely to emerge as a significant future research trend and warrants further in-depth exploration and study.