Mapping cellular senescence in heart failure: knowledge evolution, mechanistic modules, and senotherapeutic...

Cellular senescence is increasingly recognized as a mechanistic link between cardiovascular ageing, inflammatory-fibrotic remodelling, and heart failure (HF) progression. However, the knowledge structure, thematic evolution, and translational frontiers of senescence research in HF remain incompletely mapped.

This study mapped the global research landscape of cellular senescence in HF from 2005 to 2025 by integrating dual-database bibliometric analysis with BERTopic-based semantic topic modelling.

English-language articles and reviews were retrieved from the Web of Science Core Collection and Scopus. After field verification, standardization, and deduplication, 479 publications were included. VOSviewer, CiteSpace, SCImago Graphica, Pajek, Python, and Microsoft Excel were used for bibliometric and visualization analyses. PubMedBERT-based embeddings and BERTopic were applied to identify latent semantic themes from titles, abstracts, and keywords.

Publications increased rapidly after 2020, with 336 papers published between 2020 and 2025, accounting for 70.1% of the corpus. China and the United States were the leading contributors, with the United States showing higher collaboration strength and accumulated citation counts within the analysed dataset. Co-citation analysis identified foundational studies in senescence biology, senolytics, cardiovascular ageing, and HF remodelling. Keyword evolution showed a shift from oxidative stress, cardiac stem/progenitor cell senescence, and vascular cell senescence toward inflammation, metabolic remodelling, biomarkers, HF phenotypes, and senotherapeutics. BERTopic identified 17 substantive topics, with Cardiac and Cardiovascular Aging as the largest theme, followed by Cardiac Fibrosis and Fibroblast Activation, SASP-related Cardiovascular Senescence, Cardiac Regeneration, and Doxorubicin Cardiotoxicity.

Bibliometric and semantic analyses indicate growing research interest in cell-type-specific senescence, inflammatory-fibrotic remodelling, HF phenotype heterogeneity, biomarkers, and senotherapeutics. These findings highlight opportunities for integrating mechanistic research with clinical investigation. Future studies should prioritize cell-specific senescence atlases, multidimensional biomarkers, comorbidity-aware HF stratification, and cautious evaluation of senotherapeutics in HF subgroups with evidence of senescence-associated pathology.