Ferroptosis in Autoimmune Diseases: Research Advances and Therapeutic Strategies

Ferroptosis, an iron-dependent programmed cell death driven by lipid peroxidation, plays a critical role in autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, and psoriasis. This review systematically explores the interaction between ferroptosis and the immune system, highlighting its dynamic regulation of immune cell function (e.g., Treg cell stability, neutrophil activity) and inflammatory microenvironments via signaling pathways including JAK/STAT and NF-κB. Ferroptosis suppresses inflammation in rheumatoid arthritis by eliminating pro-inflammatory synoviocytes but exacerbates tissue damage in systemic lupus erythematosus through neutrophil ferroptosis. While ferroptosis inhibitors (e.g., Fer-1) and inducers (e.g., IKE) show promise in preclinical models, clinical translation faces challenges such as disease-specific mechanistic heterogeneity, insufficient drug selectivity, and complex metabolic interactions. Future research should integrate multi-omics, organoid models, and AI-driven predictions to develop precision-targeted strategies, offering novel therapeutic paradigms for autoimmune diseases.