Guizhou Universisity of Traditional Chinese Medicine, Guiyang, China.
Department of Rheumatology and Immunology, The Affiliated Hospital of Guizhou Medical Universisity, Guiyang, China.
Front Immunol. 2024 Jul 15;15:1438803. doi: 10.3389/fimmu.2024.1438803. eCollection 2024.
Ferroptosis is an iron-dependent mode of cell death distinct from apoptosis and necrosis. Its mechanisms mainly involve disordered iron metabolism, lipid peroxide deposition, and an imbalance of the antioxidant system. The endoplasmic reticulum is an organelle responsible for protein folding, lipid metabolism, and Ca regulation in cells. It can be induced to undergo endoplasmic reticulum stress in response to inflammation, oxidative stress, and hypoxia, thereby regulating intracellular environmental homeostasis through unfolded protein responses. It has been reported that ferroptosis and endoplasmic reticulum stress (ERS) have an interaction pathway and jointly regulate cell survival and death. Both have also been reported separately in rheumatoid arthritis (RA) mechanism studies. However, studies on the correlation between ferroptosis and ERS in RA have not been reported so far. Therefore, this paper reviews the current status of studies and the potential correlation between ferroptosis and ERS in RA, aiming to provide a research reference for developing treatments for RA.
铁死亡是一种不同于细胞凋亡和坏死的铁依赖性细胞死亡模式。其机制主要涉及铁代谢紊乱、脂质过氧化物沉积和抗氧化系统失衡。内质网是一种负责细胞内蛋白质折叠、脂质代谢和 Ca 调节的细胞器。它可以被诱导在内质网应激中，以响应炎症、氧化应激和缺氧，从而通过未折叠蛋白反应调节细胞内环境的稳态。据报道，铁死亡和内质网应激（ERS）之间存在相互作用途径，并共同调节细胞的存活和死亡。两者在类风湿关节炎（RA）机制研究中也分别被报道过。然而，目前尚未有关于 RA 中铁死亡和 ERS 之间相关性的研究。因此，本文综述了铁死亡和 ERS 在 RA 中的研究现状及其潜在相关性，旨在为开发 RA 治疗方法提供研究参考。
