Mapping the MicroRNA Landscape of Cadmium Exposure: A Bibliometric and Bioinformatics Analysis of Molecular Targets and Regulatory Pathways

Cadmium is a persistent toxic metal that promotes oxidative stress, inflammation, and epigenetic dysregulation; however, the research landscape and recurrent microRNA (miRNA)-mediated responses associated with cadmium exposure remain incompletely characterized. This study integrated bibliometric, structured content, and bioinformatics analyses to identify major research trends and recurrent miRNA signals. PubMed/MEDLINE, Scopus, and Web of Science Core Collection were searched using predefined cadmium- and miRNA-related search terms, yielding 1511 source records. After language/document-type filtering and cross-database deduplication, 817 unique records remained for screening, of which 286 publications formed the final bibliometric corpus. Author-keyword co-occurrence analysis was performed using a minimum occurrence threshold of ≥3, with ≥5 used as a sensitivity analysis. Cadmium and microRNA remained the dominant thematic core, while heavy-metal toxicity, apoptosis, and cadmium-stress responses represented the most recurrent secondary themes. In the final human-relevant biological evidence corpus (n = 32 studies), recurrent miRNAs showed substantial directional heterogeneity rather than a uniformly replicated response: miR-155 was reported in four studies with an equal number of increases and decreases, whereas the let-7 and miR-30 families showed modest downward tendencies, and miR-146b and miR-222 showed modest upward tendencies. These small study counts preclude strong claims of directional reproducibility. The miRNA–target network component should therefore be interpreted as exploratory and hypothesis-generating rather than as evidence of cadmium-specific pathway convergence. Overall, this synthesis supports a broader and more reproducible literature map while emphasizing the need for standardized exposure assessment, miRNA measurement, and independent validation of candidate regulatory signals.