Naa10p impairs PGC-1α/Pparγ2 interaction to inhibit mitochondrial protection in pancreatitis.

Naa10p disrupts the protective mitochondrial UCP1 pathway in acute pancreatitis (AP). This study demonstrates that Naa10p upregulation in AP correlates with decreased UCP1 expression and increased reactive oxygen species production. Silencing Naa10p improved cell survival, suppressed inflammation, and enhanced UCP1 levels by promoting PGC-1α/Pparγ2 interaction. Co-immunoprecipitation and luciferase assays confirmed that Naa10p inhibits UCP1 promoter activation. This study reveals the significance of Naa10p as a potential target for the treatment of AP and provides a new idea for the intervention of pancreatic inflammatory diseases.