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在糖尿病病中,CNPY2通过调节PERK/ATF4/CHAC1通路和MAM完整性来加剧管细胞亡

Jingfang Chen^1,2,3,4, Dongwei Liu^1,3,4, Lei Lei²

¹Department of Nephrology, the First Affiliated Hospital of Zhengzhou University, Research Institute of Nephrology, Zhengzhou University, Traditional Chinese Medicine Integrated Department of Nephrology，the First Affiliated Hospital of Zhengzhou University, Henan Province Research Center for Kidney Disease，the First Affiliated Hospital of Zhengzhou University, Key Laboratory of Precision Diagnosis and Treatment for Chronic Kidney Disease in Henan Province, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, P. R. China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|April 11, 2025

概括

糖尿病脏病 (DN) 涉及铁和线粒体相关的内细胞网膜 (MAM) 损伤. 覆盖FGF信号调节器2 (CNPY2) 通过PERK/ATF4/CHAC1通路促进铁和MAM干扰,从而加剧DN.

科学领域:

细胞生物学细胞生物学
腎臟病學 (nephrology) 是一種醫學專業.
分子医学是分子医学.

背景情况:

铁亡是糖尿病病 (DN) 管损伤的一个关键机制.
线粒体相关的细胞内网膜 (MAM) 完整性对细胞过程至关重要,但其在DN中的作用尚不清楚.
了解DN中铁和MAM之间的相互作用对于治疗开发至关重要.

研究的目的:

调查FGF信号调节器2 (CNPY2) 在ferroptosis和糖尿病病 (DN) 中MAM调节中的作用.
阐明 CNPY2 影响 DN 管状损伤的潜在分子机制.

主要方法:

使用了糖尿病病 (DN) 的db/db小鼠模型.
评估了管中CNPY2的表达水平.
操纵CNPY2水平 (下调和过度表达) 以评估其对铁和MAM完整性的影响.
研究了PERK/ATF4/CHAC1信号通路的激活.

主要成果:

发现CNPY2在DN模型的管中受到上调.
降低CNPY2的调节减少了铁亡,并改善了DN中的MAM完整性.
过度表达CNPY2通过增加铁亡和破坏MAM形成,使管状损伤恶化.
证实CNPY2可以激活PERK/ATF4/CHAC1通路,从而促进铁亡.

结论:

在糖尿病病 (DN) 进展期间,CNPY2在调节铁和MAM完整性方面发挥着重要作用.
CNPY2通过PERK/ATF4/CHAC1信号通路进行作用,以调解DNA中的铁和管状损伤.
CNPY2代表了治疗糖尿病病 (DN) 的潜在治疗标.

关键词:

吊顶 FGF信号调节器2 (CNPY2) 的信号调节器糖尿病性脏病糖尿病脏病细胞内膜网膜 (ER) 的压力压力.铁性化 (ferroptosis) 是一种线粒体关联的内等质网膜 (MAM)

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