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酸通过TGF-β1 / Smad / ROS信号通路加剧足细胞损伤

Miao Jia¹, Lihua Lin¹, Kang Xun¹

¹Department of Nephrology, The People's Hospital of Suzhou New District, Suzhou, China.

Kidney & blood pressure research

|May 12, 2024

概括

内氧硫酸盐 (IS) 通过增加氧化应激和改变 podocytes 中的 TGF-β1 / Smad 信号,使糖尿病病变得更糟. 这项研究揭示IS影响关键蛋白质,为糖尿病病提供了新的治疗标.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
糖尿病学糖尿病学
分子生物学分子生物学

背景情况:

糖尿病病是由高血糖诱导的活性氧物种 (ROS) 和转化生长因子β1 (TGF-β1) /Smad信号驱动的.
内氧硫酸盐 (IS) 是一种来自肠道的尿性毒素,通过氧化应激和炎症加剧了podocyte损伤.
对于TGF-β1信号传递在糖尿病病中IS诱导的细胞损伤中的确切作用仍然不完全理解.

研究的目的:

为了研究印硫酸盐 (IS) 对细胞损伤标记物的影响.
阐明反应性氧物种 (ROS) 和转化生长因子β1 (TGF-β1) /Smad信号通路在IS介导的细胞损伤中的参与.
通过了解IS效应,探索糖尿病病的潜在治疗策略.

主要方法:

在体外培养的分化大鼠细胞.
使用定量实时PCR (qRT-PCR) 和西式涂抹来测量蛋白质和基因表达水平.
操纵TGF-β1水平 (沉默和过度表达),使用ROS抑制剂 (乙半氨酸),并暴露细胞高葡萄糖 (HG) 和IS.

主要成果:

高葡萄糖 (HG) 条件,当与TGF-β1沉默或ROS抑制相结合时,可调节上升的保护性细胞标记物 (尼林,合成,CD2AP,SRGAP2a) 和调节下降的α-SMA.
相反,TGF-β1过度表达的HG降低了保护标记的调节和升高了α-SMA.
在HG条件下的IS补充剂显著减少了保护标记,改变了Smad信号组件 (Smad2/3,p-Smad2/3,Smad7),影响了NOX4表达,并增加了ROS产量.

结论:

酸 (IS) 显著导致糖尿病病中的细胞损伤.
通过调节ROS的产生和TGF-β1/Smad信号通路,IS调节关键细胞蛋白的表达.
这些发现为开发针对IS,ROS和TGF-β1/Smad途径的糖尿病病治疗提供了新的理论支持.

关键词:

印度硫酸盐的含量是多少?足细胞的损伤.这就是ROSOS ROS.在TGF-β1/Smad信号系统中.

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