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由V-ATPase相互作用蛋白NCOA7介导的压力颗粒清除减轻了卵巢衰老

Ting Dong^1,2, Nianyu Li^{3,4,5,6,7,8,9,10}, Huirui Wang¹¹

¹Department of Natural Products Chemistry, Key Lab of Chemical Biology of the Ministry of Education, Shandong University, Jinan, China. tingdong2021@sdu.edu.cn.

|July 31, 2025

概括

核受体联合激活剂7 (NCOA7) 缺乏通过损害压力颗粒清除来加速卵巢衰老. 恢复NCOA7功能或增强粒细胞可以缓解细胞衰老和延迟卵巢衰老.

科学领域:

生殖生物学生殖生物学
细胞衰老细胞衰老
衰老的研究研究.

背景情况:

生殖寿命对于女性的生育能力和健康的衰老至关重要.
压力反应,特别是压力颗粒积累在卵巢衰老中的作用尚不清楚.
目前缺乏有效的卵巢衰老干预措施.

研究的目的:

调查核受体辅激剂7 (NCOA7) 在卵巢衰老中的作用.
阐明NCOA7影响卵巢中压力颗粒动态和细胞衰老的机制.
为了确定减轻卵巢衰老的潜在治疗点.

主要方法:

在卵巢衰老的女性中发现了NCOA7的突变和减少表达.
利用NCOA7删除小鼠模型研究其对卵巢衰老和生育能力的影响.
研究了NCOA7在压力颗粒形成和降解中的分子机制.
采用拉巴胺素和NCOA7mRNA输送来调节粒细胞并评估其对细胞衰老和卵巢衰老的 in vitro 和 in vivo 影响.

主要成果:

在经历卵巢衰老的妇女中观察到有害突变和减少NCOA7表达.
在小鼠中,NCOA7删除加速了氧化应激诱导的细胞衰老,卵巢衰老和降低生育能力.
通过与G3BP1-V-ATPase相互作用,NCOA7促进了压力颗粒的自降解.
通过拉巴胺素或NCOA7mRNA传递增强粒细胞缩,加速压力颗粒的清除,缓解颗粒细胞衰老,并延迟小鼠的卵巢衰老.

结论:

通过调节压力颗粒清除,NCOA7在维持卵巢抗压能力方面发挥着至关重要的作用.
压力颗粒降解的NCOA7介导途径代表了一种影响卵巢衰老的新机制.
向颗粒或恢复NCOA7功能提供了潜在的治疗策略,以缓解卵巢衰老和支持女性生殖健康.

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