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Deletion of the core transcription factor BMAL1 exacerbated the severity of colitis. However, the underlying molecular mechanisms of BMAL1 in UC remain unclear. We found that BMAL1 was downregulated in UC tissues and in LPS\u2010induced MODE\u2010K cells, whereas CXCL1 was highly expressed. Overexpression of BMAL1 reduced LPS\u2010induced pyroptosis in MODE\u2010K cells and restoring the expression of ZO\u20101, Claudin\u20101, and Occludin, thereby improving intestinal epithelial barrier function. Mechanistically, BMAL1 can negatively regulate the CXCL1 expression by inhibiting the activity of its promoter. Additionally, proteomics analysis identified MEF2A as a downstream protein of BMAL1. The protective effect of BMAL1 on MODE\u2010K cells was achieved through direct negative regulation of CXCL1 or indirect negative regulation of MEF2A expression. Thus, BMAL1 plays a protective role in maintaining the integrity of the intestinal epithelial barrier and represents a potential therapeutic target for UC treatment.<\/jats:p>","DOI":"10.1155\/mi\/9930240","type":"journal-article","created":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T07:11:18Z","timestamp":1784704278000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Deletion of Circadian Rhythms Gene BMAL1 Impairs the Intestinal Epithelial Barrier and Exacerbates Intestinal Inflammation by Inducing 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