Advances in the study of ferroptosis and its relationship to autoimmune diseases.

ABSTRACT

Ferroptosis represents a novel mode of programmed cell death characterized by the intracellular accumulation of iron and lipid peroxidation, culminating in oxidative stress and subsequent cell demise. Mounting evidence demonstrates that ferroptosis contributes significantly to the onset and progression of diverse pathological conditions and diseases, including infections, neurodegenerative disorders, tissue ischemia-reperfusion injury, and immune dysregulation. Recent investigations have underscored the pivotal role of ferroptosis in the pathogenesis of rheumatoid arthritis, ulcerative colitis, systemic lupus erythematosus, and asthma. This review provides a comprehensive overview of the current understanding of the regulatory mechanisms governing ferroptosis, particularly its interplay with iron, lipid, and amino acid metabolism. Furthermore, we explore the implications of ferroptosis in autoimmune diseases and deliberate on its potential as a promising therapeutic target for diverse autoimmune disorders.