曼诺斯通过由代谢物GlcNAc-6P激活的AMPK来对抗GSDME介导的火灭菌
Yuan-Li Ai1, Wei-Jia Wang2, Fan-Jian Liu1
1State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian, China.
Cell research
|July 17, 2023
概括
简单的糖类曼诺,通过激活AMP激活蛋白激酶 (AMPK) 来抑制一种叫做热亡的细胞死亡途径. 这一发现表明,曼诺糖可以减少化疗的副作用.
科学领域:
- 细胞生物学 细胞生物学
- 生物化学 生化学
- 免疫学 免疫学 免疫学
背景情况:
- 热致死是一种调节的细胞死亡途径,涉及气皮蛋白质.
- 气体皮质胺中介性热灭菌的负调节机制尚未完全理解.
研究的目的:
- 为了研究曼诺斯在GSDME介导的灭中的抑制机制.
- 探索曼诺斯在缓解化疗诱导的组织毒性的治疗潜力.
主要方法:
- 在细胞和小鼠模型中研究了曼诺斯对热的作用.
- 使用AMPK淘汰和GSDME淘汰老鼠来确认调节途径.
- 在小鼠癌症模型和接受化疗的小患者队列中评估了曼诺斯的使用.
主要成果:
- 曼诺斯通过N-乙糖胺-6-酸盐 (GlcNAc-6P) 激活AMP激活蛋白激酶 (AMPK).
- 激活的AMPK酸化了GSDME,阻断了它的裂变并抑制了热亡.
- 在小鼠和患者中,曼诺的使用减少了化疗诱导的组织损伤,但没有影响抗瘤功效.
结论:
- 曼诺斯通过AMPK激活来对抗GSDME介导的热,揭示了一个新的调节途径.
- 曼诺补充剂在临床环境中有望缓解化疗诱导的副作用.
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