单细胞桥梁的乳酸驱动的重编程 炎症性并发症中的骨损失
Junbin Wei1, Zhiqian Ye1, Deqian Tang2
1Hospital of Stomatology, Guanghua School of Stomatology, South China Center of Craniofacial Stem Cell Research, Guangdong Provincial Key Laboratory of Stomatology, Sun Yat-sen University, Guangzhou 510055, China.
Biomolecules
|February 27, 2026
概括
血中乳酸酸的升高与牙周炎和类风湿性关节炎中的炎症和骨损失有关. 关键基因SAT1,TET2和HIF1A可能作为这些炎症性骨疾病的生物标志物.
科学领域:
- 免疫代谢过程中的免疫代谢.
- 骨生物学 骨生物学 骨生物学
- 慢性炎症疾病 慢性炎症疾病
背景情况:
- 炎症性骨损失在牙周炎 (PD) 和类风湿性关节炎 (RA) 中很常见.
- 这些不同的疾病共享免疫介导的骨再吸收机制.
- 了解分子驱动因素对于治疗并发性炎症性骨损失至关重要.
研究的目的:
- 在并发性炎症疾病中识别骨损伤的分子驱动因素.
- 调查乳酸代谢在PD和RA病变发生过程中的作用.
- 寻找潜在的生物标志物用于与炎症相关的骨损失.
主要方法:
- 使用PD和RA模型进行生物信息分析和实验验证.
- 单细胞RNA对PD和RA队列的测序.
- 机器学习来识别与乳酸相关的核心基因 (SAT1,TET2,HIF1A).
- 在体内和体外功能测定.
主要成果:
- 血中乳酸盐水平升高与PD和RA模型中的疾病严重程度相关.
- 乳酸代谢基因在单细胞中被上调,与炎症和骨质细胞生成有关.
- SAT1,TET2和HIF1A显示出这两种疾病的诊断潜力.
- 乳酸重新编程单细胞,将免疫激活与骨再吸收联系起来.
结论:
- 乳酸驱动的免疫代谢轴连接免疫反应和骨重塑.
- SAT1,TET2和HIF1A被确定为与炎症相关的骨损失的潜在生物标志物.
- 向乳酸代谢可能为并发性炎症性骨病提供治疗策略.
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