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Btg2通过Smad3-依赖的细胞-半机细胞过渡促进焦点细分细胞凝结症

Qiong- Dan Hu^1,2,3,4, Hong-Lian Wang¹, Jian Liu^3,5

¹Research Center of Integrated Traditional Chinese and Western Medicine, the Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Sichuan, 646000, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|September 26, 2023

概括

B细胞转位基因2 (Btg2) 通过促进细胞-介质细胞过渡,驱动着焦点细分结核硬化 (FSGS). 准Btg2可能为FSGS进展提供治疗策略.

科学领域:

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

背景情况:

足细胞损伤是焦点细分型淋巴结核病 (FSGS) 进展的核心.
了解驱动小细胞损伤的分子机制对于开发有效的治疗方法至关重要.

研究的目的:

调查B细胞转位基因2 (Btg2) 在阿德里亚胺素 (ADR) 诱导的FSGS中的作用.
阐明Btg2通过该信号通路调解受细胞损伤的信号通路.

主要方法:

在FSGS患者和动物模型中分析Btg2表达.
研究Btg2缺失或过度表达对细胞上皮质-介质细胞过渡 (EMT) 的 in vitro 和 in vivo 影响.
检查Btg2,Smad3和TGF-β1信号传递之间的相互作用.

主要成果:

Btg2在FSGS中的细胞上调调节,与损伤相关.
在ADR治疗的小鼠中,细胞特异性的Btg2缺失改善了蛋白尿和血球硬化.
Btg2通过Smad3依赖的途径促进TGF-β1诱导的细胞EMT和纤维化.

结论:

在FSGS中,Btg2通过促进Smad3依赖的细胞-介质细胞过渡来发挥病原性作用.
一个TGF-β/Smad3-Btg2信号电路有助于FSGS中的细胞损伤.
Btg2抑制是FSGS的一个潜在的治疗点.

关键词:

在 Btg2 中.在TGF-β/Smad3信号传输中.表皮细胞-介质细胞过渡.焦点细分型淋巴结核硬化这是一个podocyte.

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