骨关节炎中铁下垂和免疫衰老之间的潜在相互作用：来自骨免疫微环境的证据整合和翻译见解
Potential crosstalk between ferroptosis and immunosenescence in osteoarthritis: evidence integration and translational insights from the osteoimmune microenvironment.
摘要(中文译文)
骨关节炎（OA）传统上被视为一种以软骨磨损为主要特征的退行性疾病。然而，越来越多的证据表明，它本质上是一种全关节疾病，涉及软骨、滑膜、软骨下骨和免疫成分的协同参与。近年来，铁死亡和免疫衰老各自被认定为OA发生和进展的促进因素，但二者在骨免疫微环境中的潜在相互作用仍未得到充分整合。本综述总结了铁稳态失衡、脂质过氧化和抗氧化防御受损如何促进关节驻留细胞发生铁死亡，以及免疫衰老如何通过慢性低度炎症和功能重塑影响关节稳态。本综述进一步分析了这两种过程在软骨、滑膜、软骨下骨及相关免疫细胞中可能存在的交互作用。此外，本综述概述了治疗策略的当前进展，包括抗铁死亡干预、抗衰老调节以及局部递送方法的优化。目前，支持铁死亡与免疫衰老在OA中形成稳定因果循环的直接证据仍然有限，许多所提出的机制在很大程度上仍来源于研究、动物模型以及其他疾病背景下的外推。因此，本综述旨在从骨免疫微环境和证据分层的角度，为理解OA中铁死亡与免疫衰老之间的联系提供一个可检验的工作框架，并为未来以机制为导向的治疗策略的开发提供参考。
Abstract
Osteoarthritis (OA) has traditionally been regarded as a degenerative disease primarily characterized by cartilage wear and tear. However, accumulating evidence suggests that it is fundamentally a whole-joint disorder involving the coordinated participation of cartilage, synovium, subchondral bone, and immune components. In recent years, ferroptosis and immunosenescence have each been recognized as contributors to OA initiation and progression, yet their potential interplay within the osteoimmune microenvironment remains insufficiently integrated. This review summarizes how iron homeostasis imbalance, lipid peroxidation, and impaired antioxidant defense promote ferroptosis in joint-resident cells, and how immunosenescence influences joint homeostasis through chronic low-grade inflammation and functional remodeling. It further analyzes the possible crosstalk between these two processes in cartilage, synovium, subchondral bone, and related immune cells. In addition, this review outlines current advances in therapeutic strategies, including anti-ferroptotic interventions, anti-senescence modulation, and optimization of local delivery approaches. At present, direct evidence supporting a stable causal loop between ferroptosis and immunosenescence in OA remains limited, and many of the proposed mechanisms are still largely derived from studies, animal models, and extrapolation from other disease contexts. Therefore, this review aims to provide a testable working framework for understanding the link between ferroptosis and immunosenescence in OA from the perspective of the osteoimmune microenvironment and evidence stratification, and to offer reference for the development of future mechanism-oriented therapeutic strategies.
如何引用
AMA
Jinglin Li, Fuyin Yang, Xuan Deng, Lin Zhang, Xianpeng Huang, Yang Yu, et al. Potential crosstalk between ferroptosis and immunosenescence in osteoarthritis: evidence integration and translational insights from the osteoimmune microenvironment.. Frontiers in immunology. 2026; doi:10.3389/fimmu.2026.1824999.
APA
Jinglin Li, Fuyin Yang, Xuan Deng, Lin Zhang, Xianpeng Huang, Yang Yu, et al (2026). Potential crosstalk between ferroptosis and immunosenescence in osteoarthritis: evidence integration and translational insights from the osteoimmune microenvironment.. Frontiers in immunology. https://doi.org/10.3389/fimmu.2026.1824999
GB/T 7714
Jinglin Li, Fuyin Yang, Xuan Deng, Lin Zhang, Xianpeng Huang, Yang Yu, et al. Potential crosstalk between ferroptosis and immunosenescence in osteoarthritis: evidence integration and translational insights from the osteoimmune microenvironment.[J]. Frontiers in immunology, 2026 doi:10.3389/fimmu.2026.1824999.
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