The global landscape, knowledge base, and therapeutic frontiers of cellular senescence research in pulmonary fibrosis: a multi-database bibliometric and visualization analysis

Background Pulmonary fibrosis comprises a heterogeneous group of disorders characterized by progressive scarring of the lung parenchyma and declining pulmonary function. Cellular senescence has emerged as a key mechanism linking age-related injury, dysregulated tissue repair, and persistent fibrotic progression. This study aimed to systematically characterize the global research landscape, knowledge base, thematic evolution, and therapeutic frontiers of cellular senescence research in pulmonary fibrosis. Methods We searched the Web of Science Core Collection, Scopus, and PubMed for English-language original articles and reviews published from January 1, 2001, to December 31, 2025. After cross-database deduplication, relevance screening, and bibliographic standardization, 736 publications were included. R, VOSviewer, and CiteSpace were used to analyze publication trends, collaboration among countries/regions, institutions, and authors, bibliographic coupling among source journals, reference co-citation, keyword clustering, and citation and keyword bursts. Results The earliest relevant publication appeared in 2003, and annual output accelerated markedly after 2019. Publication output increased exponentially from 2003 to 2025, with a compound annual growth rate of 20.2% ( P < 0.0001). The United States ranked first in publication output, total citations, and collaborative connectivity, whereas China showed the most rapid growth in recent years. The University of Pittsburgh and Mauricio Rojas were the most productive institution and author, respectively, and the International Journal of Molecular Sciences published the largest number of articles. Co-citation and burst analyses identified telomere dysfunction, redox imbalance, and senescence of alveolar epithelial cells and fibroblasts as the principal knowledge base; single-cell and transcriptomic approaches, epigenetic regulation, and senescence-targeted therapies represented active research frontiers. Conclusion Research on cellular senescence in pulmonary fibrosis is progressing from the delineation of fundamental mechanisms toward multi-omics-based stratification and senescence-targeted intervention. Future studies should strengthen international and interinstitutional collaboration, standardize multiparametric criteria for identifying cellular senescence and harmonize data-processing procedures, and advance translation through cell-type-specific mechanistic validation, long-term safety assessment, and prospective clinical studies.