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OLP was induced in mice by transplanting human OLP lesions into the backs of thymus\u2010free mice, and an in\u00a0vitro cell model was constructed using LPS\u2010stimulated HaCaT cells. Gene intervention was performed using shRNA lentiviral vectors. The secretion of the pro\u2010inflammatory factors IL\u20106 and TNF\u2010\u03b1, as well as the rate of apoptosis in HaCaT cells, was also assessed. ChIP assay and dual\u2010luciferase assay were used to validate the transcriptional regulation of S100A7 by nuclear factor 1 A\u2010type (NFIA). The expression of S100A7 was significantly elevated in the lesion tissues of OLP\u2010induced mice. Knockdown of S100A7 alleviated inflammation and reduced keratinocyte apoptosis. The transcription factor NFIA repressed S100A7 expression by binding to the S100A7 promoter. The overexpression of NFIA ameliorated inflammation in\u00a0vivo and reduced apoptosis in\u00a0vitro, which was abrogated by further overexpression of S100A7. Overall, our results indicate that NFIA reduces inflammatory response\u2010induced keratinocyte apoptosis in OLP by inhibiting S100A7 transcription.<\/jats:p>","DOI":"10.1002\/kjm2.70052","type":"journal-article","created":{"date-parts":[[2025,6,25]],"date-time":"2025-06-25T12:39:43Z","timestamp":1750855183000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Deletion of <scp>NFIA<\/scp> Leads to Activation of <scp>S100A7<\/scp> and Inflammatory Response\u2010Induced Apoptosis of Keratinocytes in Oral Lichen Planus Progression"],"prefix":"10.1002","volume":"41","author":[{"given":"Maimaiti","family":"Tudi","sequence":"first","affiliation":[{"name":"Department of Stomatology The First People's Hospital of Kashi  Kashi Xinjiang People's Republic of China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zumulaiti","family":"Aierken","sequence":"additional","affiliation":[{"name":"Department of 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