Exploring Ferroptosis in Allergic Inflammatory Diseases: Emerging Mechanisms and Therapeutic Perspectives

Ferroptosis, a unique form of regulated cell death driven by iron accumulation and lipid peroxidation, has emerged as a critical process in various diseases. Recent evidence suggests its involvement in the pathogenesis of allergic diseases, including asthma, allergic rhinitis, and atopic dermatitis. These conditions are characterized by chronic inflammation, oxidative stress, and immune dysregulation, all of which intersect with the molecular mechanisms of ferroptosis. Key regulators, such as glutathione peroxidase 4 (GPX4), the cystine/glutamate antiporter system Xc-, and iron metabolism pathways, play pivotal roles in ferroptotic processes and their contribution to allergic disease progression. This review explores the mechanistic link between ferroptosis and allergic diseases, emphasizing how oxidative damage and iron overload exacerbate inflammation and tissue injury. We also highlight emerging diagnostic biomarkers, including lipid peroxidation products and iron regulators, which could improve disease monitoring and stratification. Therapeutic strategies targeting ferroptosis, such as GPX4 activators, iron chelators, and lipid peroxidation inhibitors, show promise in preclinical\ studies, offering potential new avenues for treating allergic diseases. However, challenges remain in translating these findings into clinical applications. By integrating current knowledge, this review underscores the need for further research into ferroptosis as both a biomarker and therapeutic target in allergic diseases.