蛋白质学揭示了牙周炎驱动的氧化应激和NAFLD中脂质代谢障碍
Boyuan Sun1, Xiaomeng Liu1, Yixuan Jiang1
1Department of Stomatology, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Frontiers in endocrinology
|September 15, 2025
概括
牙周炎通过增加氧化应激和破坏脂质代谢,使非酒精性脂肪性肝病 (NAFLD) 恶化. 像ACOX1,DBT,ACAA2和HADHA这样的关键蛋白质被确定为NAFLD的潜在治疗标.
科学领域:
- 肝病学 肝病学是一种肝病学.
- 口腔医学是指口腔医学.
- 代谢障碍 代谢障碍 代谢障碍
背景情况:
- 牙周炎是非酒精性脂肪性肝病 (NAFLD) 的一个日益增长的危险因素.
- 关联牙周炎和NAFLD的确切机制尚未完全理解.
- 氧化应激和脂质代谢失调是潜在的关键调解者.
研究的目的:
- 调查牙周炎如何影响NAFLD进展.
- 确定参与肝氧化应激和NAFLD中脂质变化的分子标.
- 探索特定蛋白质在牙周炎相关的NAFLD中的作用.
主要方法:
- 建立了使用关节绑定进行牙周炎的老鼠模型.
- 评估肝脏病理,脂质积累和氧化应激标志物.
- 利用蛋白质组分析识别差异表达蛋白 (DEP) 并构建蛋白质-蛋白质相互作用 (PPI) 网络.
主要成果:
- 牙周炎显著增加肝脏脂质积累,纤维化和氧化应激.
- 确定了244个涉及代谢和炎症途径的DEP.
- 发现了ACOX1,DBT,ACAA2和HADHA作为关键的枢纽蛋白,它们的下调与受损的脂质氧化和肝损伤有关.
结论:
- 牙周炎通过氧化应激和脂质代谢功能障碍加剧NAFLD.
- ACOX1,DBT,ACAA2和HADHA代表了牙周炎引起的NAFLD的潜在治疗点.
- 强调口腔健康和全身代谢疾病之间的联系,建议新的干预策略.
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