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

TL;DR

Naa10p disrupts mitochondrial protection in pancreatitis, and reducing it improves cell survival and reduces inflammation.

Contribution

The study identifies Naa10p as a novel regulator of mitochondrial protection in acute pancreatitis.

Findings

Naa10p upregulation correlates with decreased UCP1 expression and increased reactive oxygen species in pancreatitis.

Silencing Naa10p enhances PGC-1α/Pparγ2 interaction, improves cell survival, and reduces inflammation.

Naa10p inhibits UCP1 promoter activation, confirmed by co-immunoprecipitation and luciferase assays.

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.

This study identifies Naa10p as a key regulator in acute pancreatitis, linking its elevated expression to decreased UCP1 levels, mitochondrial dysfunction, and enhanced inflammation. Silencing Naa10p mitigates these effects, enhancing cell survival and reducing oxidative stress. These findings highlight Naa10p as a potential therapeutic target for pancreatitis.

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