细胞内膜网膜压力涉及高葡萄糖诱导的细胞核质细胞灭
Xiaochun Xiong1, Ying Wu2, Hengguo Long1
1Department of Orthopedics, Zhoushan Hospital of Traditional Chinese Medicine, Zhoushan, China.
Acta biochimica Polonica
|June 12, 2023
概括
糖尿病通过诱导细胞死亡加速椎间盘退化 (IDD). 高葡萄糖触发了内分泌网膜应激 (ERS),导致核 (NP) 细胞中的热亡,这一过程可以通过向ERS或热亡来减轻.
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
- 糖尿病学 糖尿病学
背景情况:
- 糖尿病是一种已知的椎间盘退化 (IDD) 风险因素.
- 糖尿病影响细胞核 (NP) 细胞的具体机制,特别是关于编程细胞死亡的具体机制,需要阐明.
研究的目的:
- 为了研究高葡萄糖诱导的NP细胞退化的pyroptosis的作用.
- 探索内细胞内糖尿病相关热的内细胞内内压力 (ERS) 的参与.
主要方法:
- 试验室高葡萄糖模型模拟NP细胞中的糖尿病状况.
- 评估细胞内膜网膜应激 (ERS) 和热的标志物 (例如IL-1β,IL-18,caspase-1).
- 在各种治疗条件下评估NP细胞活力和细胞外矩阵成分表达 (原II,亚格兰).
主要成果:
- 高葡萄糖暴露诱导了NP细胞退化,ERS和热.
- 升高的ERS加剧了热亡,而其抑制缓解了高葡萄糖诱导的热亡和NP细胞退化.
- 抑制热致死减少了NP细胞退化,但没有影响ERS水平.
结论:
- 细胞内膜网膜应激 (ERS) 在细胞核中调解高葡萄糖诱导的热.
- 向ERS或烧途径提供了一种潜在的治疗策略,以保护NP细胞免受与糖尿病相关的退化.
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