Selenium nutritional status and cardiovascular diseases: mechanisms of cardioprotection and 21 years of global research trends in precision prevention (2005-2026).

BACKGROUND: Selenium contributes to selenoprotein-dependent redox regulation, thyroid hormone metabolism, and cellular defense, but its role in cardiovascular disease remains clinically uncertain. Observational studies have associated low or atypical selenium status with adverse cardiovascular outcomes, whereas supplementation trials have generally produced neutral or inconclusive results. This study mapped the development of selenium-cardiovascular research and integrated the identified themes with a clinically oriented narrative synthesis of selenium exposure, functional biomarkers, cardiovascular phenotypes, supplementation, and safety. METHODS: Publications indexed in the Web of Science Core Collection, Scopus, PubMed, and Embase between January 1, 2005 and May 12, 2026 were retrieved. After document-type filtering, deduplication, and relevance screening, 1,133 documents were included. Publication trends, geographic and collaboration structures, journal relationships, co-cited references, keyword networks, thematic evolution, and citation bursts were analyzed using R, VOSviewer, CiteSpace, Pajek, Gephi, and Python. A descriptive design-level appraisal of the ten most locally cited documents complemented the bibliometric analyses. RESULTS: Publication output increased substantially after 2015. Earlier research emphasized selenium deficiency, Keshan disease, glutathione peroxidase activity, and antioxidant defense, whereas more recent publications increasingly addressed cardiovascular mortality, heart failure, selenoprotein P, GPX4, ferroptosis, selenium nanoparticles, environmental co-exposures, and machine learning. The evidence base showed biological coherence but translational fragmentation: mechanistic studies supported plausible selenium-sensitive pathways, observational studies identified context-dependent risk associations, and randomized evidence did not demonstrate a broadly applicable cardiovascular benefit of supplementation. Major translational challenges included inadequate stratification by baseline selenium status, inconsistent distinction among dietary intake, total circulating selenium, and functional biomarkers, heterogeneous cardiovascular endpoints, geographic variation, and insufficient consideration of nonlinear dose-response and safety relationships. CONCLUSION: Current evidence does not support universal selenium supplementation for cardiovascular prevention. A more informative research strategy is to evaluate selenium status as a context-dependent marker of nutritional and functional vulnerability and to test targeted correction in biomarker-enriched populations defined by baseline status, cardiovascular phenotype, regional nutritional context, and a prespecified safety range.