CD36限制了脂质相关的巨细胞在白色脂肪组织中的积累在动脉生成过程中
Vaya Chen1, Jue Zhang1, Jackie Chang1
1Versiti Blood Research Institute, Milwaukee, WI, United States.
Frontiers in cardiovascular medicine
|August 19, 2024
概括
功能障碍的内脏白脂肪组织 (WAT) 驱动着炎症和动脉样硬化. 通过增加WAT中的脂质相关巨细胞 (LAM) 减少炎症.
科学领域:
- 免疫学 免疫学 免疫学
- 代谢性疾病是一种代谢性疾病.
- 动脉样硬化的研究研究.
背景情况:
- 内脏白脂肪组织 (WAT) 功能障碍有助于慢性炎症和动脉样硬化.
- 脂肪组织相关的巨细胞 (ATM) 是WAT中的关键免疫细胞,但它们在动脉生成过程中的异质性尚不清楚.
- 拾尸体受体CD36在ATM通信和炎症中发挥作用.
研究的目的:
- 在饮食诱导的动脉样硬化中定义ATM异质性和表型.
- 研究CD36在ATM功能和WAT炎症中的作用.
- 为了确定新的ATM亚群及其代谢概况.
主要方法:
- 从Apoe-null小鼠获得WAT ATM的单细胞RNA测序.
- 细胞代谢和功能测试.
- 对Apoe/Cd36双零小鼠进行分析,以评估CD36的功能.
主要成果:
- 确定了一种新的ATM亚种群",不健康的巨",具有低活力和高脂质代谢.
- 在Apoe/Cd36双零小鼠中,脂质相关巨细胞 (LAM) 显著增加 (8.4倍).
- CD36缺乏导致ATM脂质吸收增加,脂肪细胞缩减少,炎症减少.
结论:
- CD36对于平衡脂质代谢和内脏WAT中的炎症至关重要.
- 缺少CD36促进LAM积累,减少WAT炎症,在动脉质条件下增强脂质代谢.
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