巨细胞表型切换和与肥胖相关的代谢风险:机制和目标
K F Hinojosa Vera1, C Hemakumar2, R S Bilachi3
1Laboratory of Experimental and Translational Medicine, Institute Multidisciplinary of Biological Research, CONICET-SL. National University of San Luis, San Luis, Argentina.
Oxidative medicine and cellular longevity
|November 25, 2025
概括
在肥胖症中,脂肪组织 (AT) 中的巨细胞转变为促炎状态,导致代谢功能障碍. 准这些免疫细胞为与肥胖相关的健康风险提供了潜在的治疗策略.
科学领域:
- 免疫学 免疫学 免疫学
- 代谢健康 代谢健康
- 脂肪组织生物学 脂肪组织生物学
背景情况:
- 肥胖与由脂肪组织 (AT) 功能障碍驱动的慢性炎症 (元炎症) 有关.
- 巨细胞是关键的免疫细胞,调节AT稳态和炎症.
研究的目的:
- 为了审查肥胖症中的巨细胞两极分化.
- 为了突出ATM的可塑性,异质性和相互作用.
- 讨论AT炎症中的调节因素和新出现的巨细胞子集.
主要方法:
- 关于肥胖症中巨细胞两极分化的文献综述.
- 对ATM的转录性可塑性和功能异质性的分析.
- 对调节性转录因子 (HIF-1α,PPARγ) 和巨子集 (CD9+,Trem2+ LAMs) 的检查.
主要成果:
- 肥胖诱导ATM表型转换为一种促炎M1形状.
- 冠状结构 (CLSs) 是AT炎症的标志.
- 像HIF-1α和PPARγ这样的转录因子调节了巨细胞的两极分化.
- 脂质相关巨细胞 (LAMs) 在AT重塑和炎症中发挥双重作用.
结论:
- 了解肥胖AT的巨细胞激活对于治疗开发至关重要.
- 向巨细胞两极分化可能会减轻与肥胖相关的代谢风险.
- 恢复AT功能需要解决巨细胞驱动的炎症.
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