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ANGPTL8通过CCL5-CCR5轴将再养与单细胞动态和代谢炎症联系在一起

Ran-Ran Kan^1,2,3, Si-Yi Wang^1,2,3, Xiao-Yu Meng^1,2,3

¹Division of Endocrinology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

|November 25, 2025

概括

ANGPTL8是一种通过再养诱导的蛋白质,通过增加单细胞水平和恶化胰岛素抵抗,驱动代谢炎症. 向ANGPTL8-CCL5-CCR5通路可以治疗与肥胖相关的代谢疾病.

科学领域:

代谢性炎症是一种代谢性炎症.
内分泌学在内分泌学.
免疫学免疫学免疫学

背景情况:

代谢性炎症与单细胞变化有关,但营养调节尚不清楚.
ANGPTL8 (Angiopoietin-like 8) 是一种通过再养诱导的肝.
它在食后单细胞动态和代谢疾病中的作用尚不清楚.

研究的目的:

研究ANGPTL8在禁食再养期间调节单细胞群中的作用.
确定ANGPTL8对代谢炎症和肥胖症胰岛素抵抗的影响.
阐明将ANGPTL8与单细胞招募和激活联系起来的分子机制.

主要方法:

在人类和小鼠的禁食再养模型中检查了ANGPTL8表达.
在肥胖小鼠中操纵肝细胞特异性ANGPTL8表达.
评估循环单细胞水平,细胞因子生产和胰岛素敏感性.
通过CCL5-CCR5信号传递,研究了ANGPTL8对巨细胞极化和单细胞招募的影响.

主要成果:

ANGPTL8的过度表达增加了单细胞和促炎性细胞因子;删除减少了它们并改善了代谢参数.
再组合的ANGPTL8通过P38信号刺激了巨细胞CCL5的产生,促进了单细胞的招募.
CCL5对抗减轻了ANGPTL8的影响;CCL5补充在缺乏的小鼠中恢复了炎症.
ANGPTL8恶化了胰岛素耐药性和葡萄糖不耐受性;删除或CCL5阻断逆转了这些影响.

结论:

ANGPTL8作为一个营养检查点,通过CCL5-CCR5轴将养状态与单细胞介导炎症联系起来.
ANGPTL8通过驱动单细胞和促炎性巨细胞激活来加剧代谢功能障碍.
针对ANGPTL8-CCL5-CCR5通路为与肥胖相关的代谢疾病提供了潜在的治疗策略.

关键词:

细胞迁移/粘附情况化学因子 (chemokines) 是一种化学物质.免疫学免疫学免疫学代谢过程中的代谢.单细胞 (Monocytes) 是一种单细胞.

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