S100A11 促进急性胰腺炎,通过上调状细胞铁代谢
Huiyun Zhu1, Hongxin Sun1, Xianzhu Zhou1
1Department of Gastroenterology, The First Affiliated Hospital of Naval Medical University, 168 Changhai Road, Shanghai 200433, China.
Mediators of inflammation
|June 20, 2025
概括
S100A11通过增加与氧化应激相关的细胞死亡过程铁亡,促进急性胰腺炎 (AP). 降低胰腺细胞中的S100A11水平提高了活力,降低了铁亡的标志物,这表明了AP的治疗标.
科学领域:
- 胃肠病学 胃肠病学
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 急性胰腺炎 (AP) 是一种胃肠道疾病,导致全身炎症和器官损伤.
- 铁亡是一种受调节的细胞死亡途径,通过调节氧化应激和炎症来加剧AP的进展.
- 在AP中S100A11表达升高,可能在疾病发病过程中发挥作用.
研究的目的:
- 研究S100A11在急性胰腺炎期间调节铁亡的作用.
- 为了确定S100A11敲击对胰腺状细胞活力和铁亡标记物的影响.
- 评估S100A11抑制对AP诱导的铁亡的体内影响.
主要方法:
- 协奏质谱 (TMT) 蛋白质组学在AP大鼠模型中确定了S100A11上调.
- 通过lentiviral介导的S100A11敲击在经过caerulein治疗的AR42J胰腺小细胞中进行.
- 腺相关病毒 (AAV) 在AP大鼠模型中用于体内S100A11敲击.
主要成果:
- S100A11 knockdown 在体外增加了细胞活力和谷氨 (GSH) 水平.
- S100A11 在胰腺细胞中降低反应性氧物种 (ROS),脂质ROS和Fe2+水平.
- 在活体中,S100A11敲击抑制了AP大鼠模型中的caerulein诱导的铁亡.
结论:
- S100A11通过上调ferroptosis促进急性胰腺炎.
- 针对S100A11可能是管理AP的新型治疗策略.
- S100A11通过ferroptosis加剧了与AP相关的氧化应激和炎症.
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