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Male Sprague Dawley rats were divided into three groups: a normal thyroid function group (sham), a levothyroxine (LT4)\u2013induced hyperthyroidism group (T4 sodium), and a hyperthyroidism group treated with a miR\u2010122\u20105p inhibitor (T4 sodium\u2009+\u2009antagomir\u2010122\u20105p). Liver tissue pathology, ferroptosis and inflammatory markers, and miR\u2010122\u20105p expression were assessed. Finally, rat hepatocytes (BRL\u20103A) were treated with carbon tetrachloride (CCL4) to explore the role of the miR\u2010122\u20105p\/CCDC6 axis in hepatocyte injury. We found that miR\u2010122\u20105p was expressed at low levels in liver tissues from hyperthyroid rats. Inhibition of miR\u2010122\u20105p aggravated liver tissue injury. Additionally, in hyperthyroid rats, inflammatory factors, iron content, and markers of ferroptosis were upregulated by miR\u2010122\u20105p inhibitors. Mechanistically, miR\u2010122\u20105p was found to bind to CCDC6 and negatively regulate CCDC6 expression. Furthermore, miR\u2010122\u20105p deletion induced hepatocyte injury by exacerbating the ferroptosis process and mitochondrial damage in CCL4\u2010treated hepatocytes, a process dependent on CCDC6 expression. The miR\u2010122\u20105p\/CCDC6 axis plays a protective role in hyperthyroidism\u2010induced liver injury and serves as a potential target for the clinical treatment of hyperthyroidism\u2010associated liver disease.<\/jats:p>","DOI":"10.1155\/ije\/7047803","type":"journal-article","created":{"date-parts":[[2026,6,23]],"date-time":"2026-06-23T07:08:08Z","timestamp":1782198488000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Deletion of miR\u2010122\u20105p Exacerbated Hyperthyroidism\u2010Induced Liver Injury by Regulating 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