脂肪组织巨细胞中的FAP表达促进肥胖和代谢炎症
Yunyun Wu1,2, Chao Wu1, Tiancong Shi1
1Department of Immunology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
概括
脂肪组织巨细胞 (ATM) 中的纤维细胞激活蛋白α (FAP) 通过招募炎症细胞来驱动肥胖和代谢功能障碍. 在ATM中抑制FAP可以改善新陈代谢健康并增加能量消耗.
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.
- 肥胖研究的研究.
背景情况:
- 脂肪组织巨细胞 (ATM) 是与肥胖相关的代谢炎症和功能障碍的核心.
- 纤维细胞激活蛋白α (FAP) 被确定为ATM中的新型标记物.
研究的目的:
- 研究FAP在ATM功能中的作用及其对饮食引起的肥胖和代谢功能障碍的贡献.
- 探索FAP作为代谢障碍的潜在治疗点.
主要方法:
- 选择性FAP缺陷在小鼠和人类的ATM.
- 高脂肪饮食 (HFD) 的养模式.
- 分析巨细胞透,基因表达 (CCL8,单胺氧化酶),北上腺素水平,脂解,能量消耗和胰岛素抵抗.
主要成果:
- 巨细胞FAP缺陷保护免受饮食诱导的肥胖,减少炎症性ATM透,并减轻肝硬化和胰岛素抵抗.
- FAP在ATM中调解CCL8表达,这对于招募促炎性巨细胞至关重要.
- 缺乏FAP增加了能量消耗和氧气消耗,与增加的北上腺素和脂解有关.
结论:
- 在饮食诱导的肥胖和代谢炎症中,FAP是以前未知的ATM功能的调节者.
- 在ATM中准FAP为代谢障碍提供了潜在的免疫治疗策略.
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