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ангиотензин (1-7) 通过调节TGF-β1 / AKT途径来减缓纤维化过程,这种调节发生在大鼠体洞穴性平滑肌细胞中

Yi Xu¹, Yifang Lu¹, Geling Liu¹

¹First Department of Endocrinology, Tangshan Gongren Hospital, Tangshan City, Hebei Province, 063000, China.

Sexual medicine

|October 17, 2025

概括

高葡萄糖会导致洞体纤维化,但 ангиотензин (1-7) 通过抑制TGF-β1 / AKT通路提供保护. 这一发现揭示了勃起功能障碍的潜在治疗点.

科学领域:

内分泌学和新陈代谢学
泌尿器科泌尿器科泌尿器科泌尿器科
分子生物学分子生物学

背景情况:

过高血糖是动脉样硬化和洞穴体纤维化的关键驱动因素.
转化生长因子-β1 (TGF-β1) 显著促进身体组织中纤维组织的发展.
这一过程可以导致正常的洞穴体被纤维组织取代.

研究的目的:

研究 ангиотензин (1-7) (Ang 1-7) 在缓解 corpora cavernosa内的纤维化中的作用.
阐明调节机制,特别是TGF-β1/AKT信号通路,涉及Ang 1-7的保护作用.

主要方法:

主要鼠体洞穴肌平肌细胞 (CCSMCs) 暴露于高葡萄糖 (HG) 条件下,有或没有Ang 1-7治疗.
使用西式涂抹测量TGF-β1,原I,TGF-β受体-I (TβRI) 和洞穴蛋白-1 (Cav-1) 的蛋白质水平.
测量了活性氧物种 (ROS),过氧酸盐 (ONOO−) 含量和细胞内含量,以评估细胞应激和信号.

主要成果:

高葡萄糖暴露显著增加了TGF-β1和原I水平,诱导了氧化应激,改变了AKT信号通路,并在CCSMC中增加了细胞内.
ангиотензин (1-7) 治疗显著减少了这些HG诱导的有害影响.
Ang 1-7的保护作用与TGF-β1的下调和氧化应激的减弱有关.

结论:

ангиотензин (1-7) 证明对CCSMCs有保护作用,防止高葡萄糖诱导的损伤.
这些有益效应通过调节TGF-β1/AKT信号通路来实现.
向TGF-β1/AKT通路为管理高血糖症相关勃起功能障碍提供了一个有前途的治疗策略.

关键词:

阳氨素 (1-7) 是一种在TGF-β1中.离子水平离子水平.在糖尿病中,糖尿病是血糖性糖尿病.有纤维化的纤维化.氧化应激是一种氧化应激.

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