Du Jie, Jiang Hai, Zhang Taizhe, Zheng Chuanming, Ji Zhong
Department of Emergency Surgery The First Affiliated Hospital of Bengbu Medical University Bengbu China.
J Cell Commun Signal. 2025 Jun 23;19(2):e70015. doi: 10.1002/ccs3.70015. eCollection 2025 Jun.
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.
Naa10p破坏急性胰腺炎（AP）中具有保护作用的线粒体解偶联蛋白1（UCP1）途径。本研究表明，AP中Naa10p的上调与UCP1表达降低及活性氧生成增加相关。沉默Naa10p可改善细胞存活、抑制炎症并通过促进过氧化物酶体增殖物激活受体γ共激活因子1α（PGC-1α）/过氧化物酶体增殖物激活受体γ2（Pparγ2）相互作用来提高UCP1水平。免疫共沉淀和荧光素酶测定证实Naa10p抑制UCP1启动子激活。本研究揭示了Naa10p作为AP治疗潜在靶点的重要性，并为胰腺炎性疾病的干预提供了新思路。
