长期人类脂肪细胞有机体的发展,表现为衰老,以应对间歇性缺氧
Yunzhou Dong1, Jingjing Wang1, Feifei Feng1
1Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN 55902.
bioRxiv : the preprint server for biology
|December 18, 2025
概括
阻塞性睡眠呼吸暂停会导致人体脂肪细胞的细胞衰老. 这项研究开发了一种新的有机体模型来研究间歇性缺氧对脂肪细胞的长期影响.
科学领域:
- 细胞生物学 细胞生物学
- 代谢障碍 代谢障碍 代谢障碍
- 衰老研究研究 衰老研究
背景情况:
- 阻塞性睡眠呼吸暂停 (OSA) 和间歇性缺氧 (IH) 与脂肪组织功能障碍,胰岛素抵抗和衰老有关.
- 现有的体外模型无法复制IH对人类脂肪细胞的长期影响.
研究的目的:
- 开发和优化一个强大的长期人类脂肪细胞有机体培养系统.
- 在试验室中模拟IH诱导的脂肪细胞衰老.
主要方法:
- 在Matrigel中嵌入了人体管血管分数 (SVF) 细胞,形成有机体.
- 器官被培养长达90天,并暴露于间歇性缺氧 (IH).
- 分析了脂肪生成,细胞衰老标志物,胰岛素信号和基因表达.
主要成果:
- 基于Matrigel的有机体系统支持长期培养 (≥90天) 人体脂肪细胞.
- IH暴露抑制了脂肪生成,减少了脂质积累,并诱导了细胞衰老的标志.
- IH损害了胰岛素信号传递和基因表达的改变,包括HIF1α和衰老标志物.
结论:
- 建立了一个可靠的平台,用于长期培养人类脂肪细胞有机体.
- 这种模型有效地回顾了IH诱导的脂肪细胞功能障碍和体外衰老.
- 该系统对于研究缺氧相关的代谢障碍和临床前查非常有价值.
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