ArticleAmerican journal of preventive cardiology2025
Neutrophil-mediated effects of S100A12 on major adverse cardiovascular events: Insights from the UK biobank.
Article in American journal of preventive cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Immuno-Metabolic Reprogramming in Metabolic Syndrome and Its Cardiovascular Complications: An Integrative Bioinformatics Study.International journal of molecular sciences · 2026Article
- Single-Cell Analysis, Spatial Transcriptomics and Molecular Docking Unveil Potential Therapeutic Targets for Carotid Atherosclerosis.Balkan medical journal · 2026Article
- Neutrophils as critical orchestrators of chronic inflammation.Cellular & molecular immunology · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: S100A12, a pro-inflammatory protein primarily secreted by neutrophils, has been implicated in vascular inflammation and atherosclerosis. However, its role in major adverse cardiovascular events (MACE) remains unclear. This study aimed to investigate the association between plasma S100A12 levels and MACE risk, and to assess the potential mediating role of neutrophil count in this relationship. Methods: We conducted a prospective cohort study using data from the UK Biobank (N = 47,106). Participants with prior MACE or missing S100A12 or neutrophil count data were excluded. MACE was defined as a composite of non-fatal myocardial infarction, non-fatal stroke, and cardiovascular death. Cox proportional hazards models were used to assess the association between S100A12 and MACE risk, adjusting for demographics, lifestyle factors, metabolic parameters, and genetic predisposition. Mediation analysis was conducted to evaluate the indirect effect of neutrophil count on this association. Results: During a median follow-up of 15.3 years, 2,250 (4.8 %) participants experienced MACE, with a total follow-up time of 695,581.4 patient-years. Higher S100A12 levels were significantly associated with an increased risk of MACE (HR: 1.115, 95 % CI: 1.050-1.183, Conclusion: Elevated S100A12 levels are independently associated with increased MACEs risk, with neutrophil count serving as a significant mediator.
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Registered trials
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