类风湿关节炎（rheumatoid arthritis， RA）作为一种多因素慢性自身免疫性疾病，其典型表现为滑膜炎症、血管翳形成、软骨破坏和骨侵蚀。尽管RA的标准化死亡率呈下降趋势，但全球RA患病率的持续上升，患病年龄的年轻化倾向，正显著加剧RA的整体负担。在祖国医学中，RA常以“痹证”论治，瘀既是RA的病理产物又作为RA的主要病机贯穿疾病的始终，是导致其迁延不愈的重要原因，故活血化瘀治法在RA治疗中具有重要地位。铁死亡是一种铁依赖性程序性细胞死亡，其主要特征是铁离子和脂质过氧化物的累积以及氧化还原系统的失衡。现代医学研究表明铁死亡通过促进炎症反应和骨破坏等机制在RA疾病进展中起重要作用，靶向铁死亡的抑制剂已被证实在RA治疗中具有潜在的治疗价值。瘀与铁死亡作为调控RA进展的重要机制，二者之间又存在着密切联系：铁离子的异常蓄积不仅与血瘀在表现症状上相吻合，还可能是血瘀形成的重要条件，而脂质过氧化又会进一步促进血瘀病理状态的形成，此外现代药理学发现活血化瘀中药有效成分可通过提高机体抗氧化能力抑制RA铁死亡的发生。因此，基于“瘀”的理论阐述RA铁死亡机制，可为活血化瘀治则治法调控铁死亡进而缓解RA进展提供新的科学依据。

Rheumatoid arthritis （RA） is a multifactorial chronic autoimmune disease characterized pathologically by synovial inflammation， pannus formation， cartilage destruction， and bone erosion. Although standardized mortality rates for RA have declined， its escalating global prevalence and trend toward earlier onset continue to substantially exacerbate the disease burden. In traditional Chinese medicine （TCM）， RA is primarily categorized under “Bi syndrome.” Within this framework， blood stasis functions not only as a pathological consequence but also as a core pathogenic mechanism that persists throughout the disease course， contributing significantly to its refractory nature. Consequently， therapeutic strategies that activate blood circulation and resolve stasis play a pivotal role in clinical management. Ferroptosis is an iron-dependent form of regulated cell death characterized primarily by intracellular iron accumulation， lipid peroxidation， and redox imbalance. Emerging evidence indicates that ferroptosis exacerbates RA pathology by driving synovial inflammation and joint destruction， highlighting targeted ferroptosis inhibition as a promising therapeutic strategy. Notably， blood stasis and ferroptosis appear to share pathophysiological overlaps in RA progression. Iron accumulation aligns with the clinical manifestations of blood stasis and may critically contribute to its development， while subsequent lipid peroxidation further aggravates stasis formation. Furthermore， pharmacological studies demonstrate that active compounds from blood-activating and stasis-resolving herbs can suppress ferroptosis in RA models by enhancing endogenous antioxidant defenses. Therefore， elucidating RA-related ferroptosis through the lens of “blood stasis” theory may provide novel scientific insights into targeting this cell death pathway， offering a mechanistic rationale for applying blood-activating and stasis-resolving therapies to mitigate RA progression.