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

IF 3.6 3区生物学 Q3 CELL BIOLOGY

Journal of Cell Communication and Signaling Pub Date : 2025-06-23 DOI:10.1002/ccs3.70015

Jie Du, Hai Jiang, Taizhe Zhang, Chuanming Zheng, Zhong Ji

引用次数: 0

Abstract

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.

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Naa10p损害PGC-1α/Pparγ2相互作用，抑制胰腺炎线粒体保护

Naa10p破坏急性胰腺炎（AP）的保护性线粒体UCP1通路。本研究表明，AP中Naa10p的上调与UCP1表达降低和活性氧产生增加相关。沉默Naa10p可通过促进PGC-1α/ ppar - γ - 2相互作用改善细胞存活、抑制炎症并提高UCP1水平。免疫共沉淀和荧光素酶检测证实Naa10p抑制UCP1启动子的激活。本研究揭示了Naa10p作为治疗AP的潜在靶点的意义，为胰腺炎性疾病的干预提供了新的思路。

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来源期刊

Journal of Cell Communication and Signaling CELL BIOLOGY-

CiteScore

6.40

自引率

4.90%

发文量

期刊介绍： The Journal of Cell Communication and Signaling provides a forum for fundamental and translational research. In particular, it publishes papers discussing intercellular and intracellular signaling pathways that are particularly important to understand how cells interact with each other and with the surrounding environment, and how cellular behavior contributes to pathological states. JCCS encourages the submission of research manuscripts, timely reviews and short commentaries discussing recent publications, key developments and controversies. Research manuscripts can be published under two different sections : In the Pathology and Translational Research Section (Section Editor Andrew Leask) , manuscripts report original research dealing with celllular aspects of normal and pathological signaling and communication, with a particular interest in translational research. In the Molecular Signaling Section (Section Editor Satoshi Kubota) manuscripts report original signaling research performed at molecular levels with a particular interest in the functions of intracellular and membrane components involved in cell signaling.