Bidirectional interaction between ferroptosis and chronic fatigue syndrome: Insights into neuroinflammation and oxidative stress

Abstract

Chronic fatigue syndrome (CFS) is a multisystem disease of unknown aetiology. It disrupts multiple physiological systems, and its pathogenesis, reliable diagnostic markers and targeted therapies remain poorly understood. Ferroptosis is a newly characterised form of programmed cell death. This cell death is associated with the pathogenesis of a variety of neurodegenerative diseases, making it a potential therapeutic target for such diseases. In this review, we focus on the interplay between CFS and ferroptosis. Relevant domestic and international literature is reviewed to summarise available findings, elucidate molecular regulatory mechanisms, and identify promising directions for future research. Our analysis reveals a bidirectional interaction between CFS and ferroptosis. Ferroptosis may contribute to CFS through oxidative stress and neuroinflammation, whereas pathological changes associated with CFS could further exacerbate ferroptosis. This review first describes the function of ferroptosis in CFS pathogenesis. Targeting ferroptosis‐related pathways may offer a potential therapeutic strategy for CFS. Nevertheless, further clinical evidence is still needed to support relevant research, and the specific regulatory network and interactions with other pathological mechanisms remain to be clarified.