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p66shc通过亡,线粒体损伤和EMT加剧了阻塞性病的进展

Xilin Gao¹, Xu Fan¹, Xiaohan Yu¹

¹Department of Pediatric Urology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, Liaoning, 110004, China; Key Laboratory of Health Ministry for Congenital Malformation, Shengjing Hospital, China Medical University, Shenyang, China.

Journal of pediatric urology

|April 15, 2025

概括

蛋白质p66shc使损伤和阻塞性病中的纤维化恶化. 沉默p66shc提供了一个潜在的策略,以减少脏纤维化在水缩的进展.

科学领域:

腎臟病學 (nephrology) 是一種醫學.
分子生物学分子生物学
病理学病理学病理学

背景情况:

水性化可以导致纤维化和功能下降.
研究了氧化还原调节蛋白p66shc在水溶解诱导的损伤中的作用.

研究的目的:

在阻塞性病中阐明p66shc在纤维化中的机制.
探索p66shc在导致损伤的细胞过程中的作用.

主要方法:

分析了小儿水缩样本中的p66shc表达.
使用完整单边尿路阻塞 (CUUO) 的小鼠模型.
在p66shc操纵后评估了细胞增殖,细胞亡,活性氧物种 (ROS),线粒体损伤和上皮-介质细胞过渡 (EMT).
在过度表达后进行了p66shc沉默和RNA测序的体内治疗效果.

主要成果:

p66shc抑制了管状上皮细胞的生长,并促进了亡.
p66shc加剧了氧化和线粒体损伤,并增强了EMT.
在体内抑制p66shc有效降低了纤维化.
RNA测序为p66shc的下游分子机制提供了洞察力.

结论:

p66shc显著导致细胞损伤和阻塞性病中的EMT.
抑制p66shc表达是一种潜在的治疗策略,可以缓解纤维化进展.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.在EMT中,EMT是EMT.线粒体损伤导致线粒体损伤.患有脏纤维化在p66shcc.

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