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由DHFR驱动的代谢记忆维持牙周组织的破坏
1State Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Journal of dental research
|June 27, 2025
概括
过高血糖会通过通过二叶酸减少酶 (DHFR) 改变巨细胞代谢,对牙周组织造成持久损伤. 恢复DHFR功能逆转了这些有害影响,这表明糖尿病并发症的新治疗点.
科学领域:
- 内分泌学 在内分泌学.
- 免疫学 免疫学 免疫学
- 牙周病学 牙周病学
背景情况:
- 糖尿病是一种全球代谢疾病,牙周组织的破坏是关键的并发症.
- 高血糖症通过代谢和免疫失调导致持续的牙周组织损伤.
研究的目的:
- 研究二叶酸减少酶 (DHFR) 在高血糖引起的慢性牙周组织破坏中的作用.
- 在糖尿病并发症的背景下探索巨细胞代谢记忆的概念.
主要方法:
- 利用小鼠模型,包括代谢记忆和骨髓移植.
- 采用了组合的代谢和转录组分析.
- 研究过高血糖症对巨细胞表型和功能的影响.
主要成果:
- 过高血糖症诱导了巨细胞的持续性炎症衰老表型,抵抗血糖控制.
- 在高血糖症下观察到降低DHFR介导的1碳代谢,降低NADP+和ATP水平.
- 过度表达DHFR成功地逆转了巨细胞中高血糖引起的代谢和病理变化.
结论:
- 巨细胞中的DHFR介导的代谢记忆是糖尿病中慢性牙周组织破坏的关键驱动因素.
- 向DHFR可能为治疗糖尿病牙周并发症提供一种新的治疗策略.
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