在衰老的核脉细胞中自降解加速椎间盘退化
Zhiqian Chen1, Chen Chen1, Xiao Yang1
1Shanghai Key Laboratory of Orthopedic Implants, Department of Orthopedics, Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, 639 Zhizaoju Road, Shanghai, 200011, P. R. China.
International journal of biological sciences
|May 10, 2024
概括
细胞衰老和炎症驱动椎间盘退化 (IDD). 我们发现,通过衰老细胞的自细胞来破坏受损的STING蛋白质降解促进了IDD,这表明增强的STING自作为治疗点.
科学领域:
- 生物医学科学 生物医学科学
- 细胞生物学 细胞生物学
- 再生医学是一种再生医学.
背景情况:
- 椎间盘退化 (IDD) 的发病包括细胞衰老和炎症.
- 干扰素基因刺激器 (STING) 轴是炎症反应的关键调解者.
研究的目的:
- 研究STING在细胞衰老和IDD中的作用.
- 在衰老的NP细胞中确定STING积累的机制.
- 探索STING自降解作为IDD的潜在治疗策略.
主要方法:
- 在衰老的NP细胞和脊椎间盘 (IVD) 中分析STING表达和自降解.
- 在正常和衰老细胞中对2'3'-cGAMP的STING激活的评估.
- 使用STINGgt/gt,cGAS-/-小鼠和大鼠尾部IVD穿孔模型进行IDD诱导.
主要成果:
- 在IDD期间,在衰老的NP细胞中观察到STING的逐渐增加.
- 功能障碍的STING自降解导致STING积累和老化NP细胞的持续炎症,促进IDD.
- 在各种IDD模型中,在衰老细胞和IVD中证实了减少STING自降解.
结论:
- 由于老化的NP细胞中自性受损的STING积累是IDD的关键驱动因素.
- 在衰老的NP细胞中准和增强STING自降解,为治疗IDD提供了一个有希望的治疗途径.
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