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通过调节LPS诱导的细胞中的PI3K/AKT通路,CIAPIN1减弱了铁亡

Ziqing Zhang¹, Jinmiao Ma¹, Minyu Shi¹

¹Department of Emergency Medicine, Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, 358 Datong Road, Pudong, Shanghai, 200137, China.

|April 21, 2025

概括

细胞因子诱导的亡抑制剂1 (CIAPIN1) 保护在脂多聚糖因子诱导的 podocytes 中的铁亡. 这通过PI3K/AKT通路发生,这表明CIAPIN1是急性损伤的治疗标.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
细胞生物学细胞生物学
分子生物学分子生物学

背景情况:

细胞因子诱导的亡抑制剂1 (CIAPIN1) 是一种已知的抗亡蛋白.
它在铁亡中的作用,特别是在脏的细胞中,尚不清楚.
铁亡是一种依赖铁的细胞死亡形式,与急性损伤 (AKI) 有关.

研究的目的:

为了研究CIAPIN1对脂聚糖 (LPS) 诱导的 podocytes 铁亡的作用.
阐明涉及CIAPIN1介导铁灭调节的分子通路.

主要方法:

血清CIAPIN1水平在患有和没有AKI的败血症患者和健康对照中进行了分析.
建立了一个使用脂聚糖 (LPS) 诱导的MPC5 podocytes的体外模型.
基因和蛋白质表达的评估使用RT-qPCR和西式涂抹.

主要成果:

血清CIAPIN1在败血性AKI患者和LPS治疗的 podocytes 中降低了调控.
过度表达CIAPIN1 (OE-CIAPIN1) 减少了LPS诱导的细胞亡和扩散.
OE-CIAPIN1激活了PI3K/AKT通路,增加了synaptopodin,降低了desmin,降低了malondialdehyde和铁水平,并上调了铁酶抑制剂SLC7A11和GPX4.
抑制PI3K/AKT可以逆转这些影响.

结论:

CIAPIN1 抑制了 LPS 诱导的 podocytes 中的铁亡.
这种保护作用通过调节PI3K/AKT信号通路来实现.
CIAPIN1代表了与败血症相关的AKI的潜在治疗标.

关键词:

急性损伤是什么?急性损伤是什么?美国中央情报局PIN1 铁化是铁化的一种.在LPS中使用LPS.在PI3K/AKT中使用.波多细胞 (Podocytes) 是一种细胞.

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