Mitochondrial damage caused by oxidative stress is a main driver of pancreatic β-cell dysfunction in the pathogenesis of type 2 diabetes mellitus. Prohibitin2 (PHB2) is a vital inner mitochondrial membrane protein that participates in mitophagy to remove the damaged mitochondria. This study aimed to investigate the role and mechanisms of PHB2-mediated mitophagy in oxidative stress-induced pancreatic β-cell dysfunction.

中文翻译：

---

氧化应激通过 Nrf2/PHB2 途径抑制 β 细胞中 PHB2 介导的线粒体自噬

氧化应激引起的线粒体损伤是 2 型糖尿病发病机制中胰腺 β 细胞功能障碍的主要驱动因素。Prohibitin2 (PHB2) 是一种重要的线粒体内膜蛋白，参与线粒体自噬以清除受损的线粒体。本研究旨在探讨 PHB2 介导的线粒体自噬在氧化应激诱导的胰腺 β 细胞功能障碍中的作用和机制。