向脂肪细胞ESRRA促进骨质生成和血管形成在脂肪细胞丰富的骨髓
Tongling Huang1, Zhaocheng Lu1, Zihui Wang1,2
1Research Center for Human Tissues and Organs Degeneration, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.
Nature communications
|May 4, 2024
概括
向脂肪细胞中的雌激素相关受体α (ESRRA) 通过减少骨髓脂肪化来保持骨的形成. 抑制ESRRA可以防止肥胖和雌激素缺乏的骨质损失.
科学领域:
- 内分泌学 在内分泌学.
- 骨生物学 骨生物学 骨生物学
- 代谢调节 代谢调节 代谢调节
背景情况:
- 过度的骨髓脂肪细胞 (BMAds) 与骨质恶化有关.
- 与雌激素相关的受体α (ESRRA) 调节了代谢应激反应.
研究的目的:
- 调查脂肪细胞特异性ESRRA在骨髓脂肪和骨形成中的作用.
- 探索ESRRA调节骨质生成和血管化的机制.
主要方法:
- 脂肪细胞特定的ESRRA淘汰赛小鼠模型.
- 雌激素缺乏和饮食诱导的肥胖模型.
- 对基因表达 (Spp1,瘦素) 和信号通路的分子分析.
- 肥胖小鼠中ESRRA的药理抑制.
主要成果:
- 脂肪细胞特异性ESRRA缺陷在高脂肪性骨髓中保留了骨质生成和血管形成.
- 缺少ESRRA增强了分泌的蛋白1 (Spp1) 和降低了叶黄素分泌.
- 废除ESRRA促进了骨髓干细胞的骨质致力和H型血管形成.
- 药理学ESRRA抑制保护肥胖小鼠免受骨质损失和骨髓脂肪化.
结论:
- 脂肪细胞ESRRA通过干扰雌激素信号传递和调节脂肪素表达来负面调节骨的形成.
- 向脂肪细胞ESRRA代表了与高骨髓脂肪相关的骨损失的潜在治疗策略.
- 抑制ESRRA建立了一个前循环,在有害的骨髓环境中促进骨形成.
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