Zheng Tengyi, Lu Fumiao, Wu Peihang, Chen Yangan, Zhang Rongxin, Li Xin
Department of Pharmacy, Guangdong Pharmaceutical University, Guangzhou, China.
School of Life Sciences and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, China.
Front Immunol. 2025 Feb 24;16:1526961. doi: 10.3389/fimmu.2025.1526961. eCollection 2025.
Periodontitis is a significant global public health issue associated with the onset and progression of various systemic diseases, thereby requiring additional research and clinical attention. Although ferroptosis and cuproptosis have emerged as significant areas of research in the medical field, their precise roles in the pathogenesis of periodontitis remain unclear. We aim to systematically summarize the current research on ferroptosis and cuproptosis in periodontal disease and investigate the roles of glutathione pathway and autophagy pathway in connecting ferroptosis and cuproptosis during periodontitis. Further, we propose that a homeostatic imbalance of copper and iron, driven by periodontal pathogens, may contribute to elevated periodontal oxidative stress, representing a potential unifying link between ferroptosis and cuproptosis involved in periodontitis. This article presents a comprehensive overview of the molecular mechanisms underlying ferroptosis and cuproptosis in periodontitis, offering novel theoretical insights into its pathogenesis and potential therapeutic targets.
牙周炎是一个重大的全球公共卫生问题,与各种全身性疾病的发生和发展相关,因此需要更多的研究和临床关注。尽管铁死亡和铜死亡已成为医学领域重要的研究方向,但其在牙周炎发病机制中的具体作用仍不清楚。我们旨在系统总结目前关于牙周疾病中铁死亡和铜死亡的研究,并探讨谷胱甘肽途径和自噬途径在牙周炎期间连接铁死亡和铜死亡中的作用。此外,我们提出,由牙周病原体驱动的铜和铁的稳态失衡可能导致牙周氧化应激升高,这代表了牙周炎中涉及的铁死亡和铜死亡之间潜在的统一联系。本文全面概述了牙周炎中铁死亡和铜死亡的分子机制,为其发病机制和潜在治疗靶点提供了新的理论见解。