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While long noncoding RNAs (LncRNAs) are established regulators, the specific mechanisms governing their roles remain largely uncharacterized. Here, we demonstrate that the LncRNA colon cancer\u2013associated transcript 1 (CCAT1) is significantly upregulated in THP1\u2010derived macrophages upon stimulation with oxidized low\u2010density lipoprotein (ox\u2010LDL). Silencing LncRNA CCAT1 markedly attenuated the ox\u2010LDL\u2010induced inflammatory response, establishing its proinflammatory function. Mechanistically, we identified miR\u2010296\u20103p as a direct downstream target of LncRNA CCAT1, which acts as a molecular sponge. This interaction was validated by dual\u2010luciferase and RNA pull\u2010down assays. Furthermore, we show that miR\u2010296\u20103p suppresses inflammation by directly targeting the mRNA of FOS\u2010like antigen 1 (FOSL1). Crucially, overexpression of LncRNA CCAT1 increased FOSL1 levels, confirming this regulatory axis. Collectively, our findings delineate a novel pro\u2010inflammatory pathway where LncRNA CCAT1 promotes macrophage inflammation by sponging miR\u2010296\u20103p, thereby derepressing its target FOSL1. Therefore, targeting LncRNA CCAT1 represents a promising therapeutic strategy for treating atherosclerotic cardiovascular disease.<\/jats:p>","DOI":"10.1155\/cdr\/9277233","type":"journal-article","created":{"date-parts":[[2025,12,23]],"date-time":"2025-12-23T07:22:17Z","timestamp":1766474537000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Knockdown of LncRNA CCAT1 Attenuates ox\u2010LDL\u2010Induced Inflammation in THP1\u2010Derived Macrophages via the miR\u2010296\u20103p\/FOSL1 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