人类丸AT1R表达的年龄相关增加及其对老老动物莱迪格细胞衰老的干预效应
Minye Zhao1, Jinhua Wei2, Yao Geng2
1Department of Gynaecology and Obstetrics, Xijing Hospital, Air Force Medical University (The Fourth Military Medical University), Xi'an 710032, P.R.China.
概括
ангиотензинII类型-1受体 (AT1R) 的激活加速莱迪格细胞衰老,并损害男性生育能力. 阻止AT1R信号传递可能为老年男性晚期发生的阴性双胞胎症提供治疗策略.
科学领域:
- 内分泌学 在内分泌学.
- 生殖生物学 生殖生物学
- 衰老研究研究 衰老研究
背景情况:
- 氨酸 - - ангиотензин系统主要通过AT1R由 ангиотензинII (AngII) 介导,影响各种生理过程.
- 随着年龄的增长,AT1R的表达和功能发生变化,影响莱迪格细胞 (LCs),并可能导致男性阴性双胞胎症.
研究的目的:
- 调查AT1R过激活在莱迪格细胞衰老中的作用及其对与年龄相关的男性阴性双胞胎症的贡献.
主要方法:
- 在老年人和老鼠丸中检查AT1R表达.
- 利用了在LC中AT1R过度表达的转基因模型.
- 评估了LC衰老,类固醇生成,精子生成,炎症和氧化应激.
- 研究了涉及MDM2,NF-κB p65和p38 MAPK的分子机制.
- 评估了老老鼠AT1R抑制的作用.
主要成果:
- 在老年丸中,AT1R表达被上调.
- 过度表达AT1R加速了LC衰老,降低了类固醇生成和精子生成,并增加了炎症和氧化应激.
- AT1R激活增强了MDM2-p65相互作用,从而以p38依赖的方式激活p65.
- 在老老鼠中,AT1R抑制改善了LC衰老和改善了丸功能.
结论:
- 丸LC中的AT1R强迫表达促进了与衰老相关的特征和雄性动物的生育能力受损.
- 阻断Ang II/AT1R通路可能是一个可行的治疗方法,用于老年男性晚期发生的阴性双胞胎症.
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