人体常驻肝脏髓状细胞可以防止肥胖的代谢压力
Emelie Barreby1, Benedikt Strunz1, Sebastian Nock1
1Center for Infectious Medicine (CIM), Department of Medicine Huddinge, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Nature metabolism
|July 6, 2023
概括
肥胖会减少人类肝脏中保护性肝脏骨髓状细胞2 (LM2). 恢复这些细胞可以对抗非酒精性脂肪肝疾病 (NAFLD) 的代谢功能障碍和氧化应激.
科学领域:
- 免疫学 免疫学 免疫学
- 肝病学 肝病学是一种肝病学.
- 代谢性疾病研究研究.
背景情况:
- 在与肥胖相关的非酒精性脂肪性肝病 (NAFLD) 中,肝细胞巨细胞的作用和周转率尚不清楚.
- 肥胖症对NAFLD发展和进展为肝硬化有很大的风险.
研究的目的:
- 为了确定在肥胖期间参与代谢健康的特定人肝骨髓状细胞种群.
- 在NAFLD风险的背景下调查这些细胞的营业额和功能.
主要方法:
- 单细胞技术和流动细胞测量被用来分析肝脏骨髓细胞在接受肝移植的个体.
- 人类2D和3D细胞培养被用于功能验证.
主要成果:
- 鉴定出一种居住性肝髓状细胞的保护子集,称为肝髓状细胞2 (LM2).
- 在肥胖个体中,LM2比例下降.
- 在肝细胞中,LM2的存在减轻了与肥胖相关的氧化应激.
结论:
- 肝脏髓状细胞的循环在人类和小鼠之间有所不同.
- 在肥胖中,LM2对代谢障碍起着保护作用.
- 准居住性髓状细胞,特别是LM2,可能是减少NAFLD氧化应激的治疗策略.
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