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向ROCK1/YAP1轴通过稳定SIRT1-依赖的线粒体动力学来改善炎症诱导的前列腺增生

Dongxu Lin¹, Pengyu Wei¹, Mengyang Zhang²

¹Department and Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Cell proliferation

|July 5, 2025

概括

向ROCK1/YAP1通路可以对抗良性前列腺激增症 (BPH) 的进展. 这项研究表明,抑制ROCK1或YAP1可以缓解BPH模型中的炎症,增生和纤维化.

科学领域:

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
病理学病理学病理学

背景情况:

良性前列腺增生 (BPH) 是老年男性普遍存在的疾病,常常因慢性炎症和氧化应激而恶化.
由ROCK1调节的YAP1蛋白在器官大小,细胞平衡和纤维化方面发挥作用,这表明它可能参与BPH病变发生.

研究的目的:

研究向ROCK1/YAP1信号轴以缓解BPH进展的治疗潜力.
阐明YAP1激活在炎症条件下促进BPH发展的分子机制.

主要方法:

通过腺相关病毒 (AAV) 注射,老鼠经历了前列腺特异性的YAP1过度表达.
建立了一个实验性自身免疫性前列腺炎 (EAP) 模型,并用ROCK1抑制剂 (fasudil) 和YAP1抑制剂 (verteporfin) 进行治疗.
细胞模型被用来确认YAP1在线粒体功能中的作用.

主要成果:

过度表达YAP1诱导了BPH表型,包括炎症,增生,纤维化和氧化应激.
在EAP模型中,用fasudil和verteporfin治疗显著缓解了BPH病变.
YAP1的激活抑制了SIRT1,损害了线粒体动力学 (DRP1/MFN2) 并加剧了氧化应激.

结论:

炎症驱动的ROCK1/YAP1轴的激活通过增加氧化应激和损害线粒体功能来促进BPH.
向ROCK1或YAP1为治疗炎症性BPH提供了一个有希望的临床前策略.

关键词:

一个SIRT1系统.一个YAP1一个YAP1 良性前列腺增生症良性前列腺增生症这是一种炎症炎症炎症炎症.线粒体的动力学

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