1. Academic Validation
  2. Identification of natural killer cell-characteristic genes in atherosclerosis based on bioinformatics analysis

Identification of natural killer cell-characteristic genes in atherosclerosis based on bioinformatics analysis

  • Sci Rep. 2025 May 16;15(1):17112. doi: 10.1038/s41598-025-98524-9.
Lei Yang # 1 Huipeng Zhang # 2 Linyan Huang 2 Ruixue Wang 2 Zhen Zhang 3 Yi Zeng 4
Affiliations

Affiliations

  • 1 Department of Nutrition, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China.
  • 2 Department of Endocrinology, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China.
  • 3 Department of Endocrinology, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China. zzhen311@163.com.
  • 4 Department of Endocrinology, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China. zengyi199@163.com.
  • # Contributed equally.
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.

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