ArticleScientific reports2025
Identification of natural killer cell-characteristic genes in atherosclerosis based on bioinformatics analysis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Endothelial cells modulate immune cell responses during atherosclerosis.Trends in immunology · 2026Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis (AS), a chronic inflammatory disease with autoimmune components, represents the predominant pathological change underlying cardiovascular diseases. Natural killer (NK) cells, pivotal actors in the innate immune system, play intricate regulatory roles in AS. Our objective was to identify and analyze NK cell-related genes involved in AS pathogenesis. We conducted differential expression analysis and functional enrichment analysis via microarray datasets from AS patients, identified NK cell-characteristic genes and performed subgroup analysis of AS on the basis of the expression levels of these genes. The results revealed that the differentially expressed genes in AS were predominantly associated with immune response activities and were significantly enriched in NK cell-mediated cytotoxicity pathways. PTPN6, ITGAL, TYROBP, SLAMF7, LCP2, HCST, HAVCR2, and VAV3 were identified as NK cell-characteristic genes. Subgroup analysis indicated that in patients with high expression levels of NK cell-characteristic genes, the progression of AS may be driven primarily by immune cell activity, whereas in those with low expression levels, TGF-β signaling may be the primary driving factor. In summary, our findings emphasize the crucial role of NK cell-mediated immunity in AS, offering potential targets for personalized immunomodulatory therapies and highlighting the need for tailored treatments based on different AS subtypes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.