亡的媒介:从细胞死亡到代谢调节
Xiaoqin Wu1,2, Laura E Nagy1,3,4, Jérémie Gautheron5
1Northern Ohio Alcohol Center, Department of Inflammation and Immunity, Cleveland Clinic, Cleveland, OH, USA.
EMBO molecular medicine
|January 9, 2024
概括
亡,一个被编程的细胞死亡过程,也调节了新陈代谢. 这篇评论探讨了细胞死亡之外的亡及其在肥胖和糖尿病等代谢疾病中的作用.
科学领域:
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
- 代谢性疾病研究研究
背景情况:
- 亡是一种被编程的细胞死亡途径.
- 像RIPKs和MLKL这样的关键介质在细胞死亡之外也有其作用.
- 失调的亡与代谢障碍有关.
研究的目的:
- 审查死细胞灭亡在细胞死亡和代谢调节中的双重作用.
- 探索死细胞灭绝在代谢疾病中的参与.
- 为了突出治疗机会.
主要方法:
- 关于亡和代谢疾病研究的文献综述.
- 对RIPK和MLKL功能的研究分析.
- 综合证据,将亡与代谢功能障碍联系起来.
主要成果:
- 亡媒介 (RIPK,MLKL) 调节能量,葡萄糖和脂质代谢.
- 异常亡有助于肥胖,糖尿病,MASLD和ALD.
- 亡会影响代谢疾病中的炎症和组织损伤.
结论:
- 亡具有显著的非亡功能,影响新陈代谢.
- 向亡可能为代谢性疾病提供新的治疗策略.
- 需要进一步的研究,以充分阐明亡-代谢相互作用.
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