Identification of Serum Level of Glutathione Peroxidase 4

Ferroptosis, first reported by Dixon et al. in 2012, is a form of non-apoptotic cell death driven by iron-dependent lipid reactive oxygen species (ROS) and accelerated by the accumulation of lipid peroxides, ultimately leading to oxidative damage to phospholipid membranes and cell death . Ferroptosis could be induced by iron metabolism disorder, lipid peroxidation accumulation, deficiency of glutathione (GSH) and inactivation of the antioxidant enzyme glutathione peroxidase 4 (GPX4). The morphological features of ferroptotic cells manifest as an aberrant mitochondrial ultrastructure, including a reduction in mitochondrial volume, an increase in mitochondrial membrane density, and the disappearance of mitochondrial cristae in ferroptotic cells . Recent studies have increasingly reported on complex associations between ferroptosis and the immune system . The regulatory activity of ferroptosis in immune function and inflammation is multifaceted and involves innate, acquired, and autoimmunity. Accumulating evidence in recent times has shown an association of ferroptosis with the pathogenesis and development of autoimmune diseases . Spondyloarthropathy comprises a group of chronic inflammatory rheumatic diseases, including ankylosing spondylitis, reactive arthritis (Reiter syndrome), arthritis or spondylitis associated with inflammatory bowel disease, and psoriatic arthritis, as well as undifferentiated spondyloarthritis. These afflictions predominantly affect the axial skeleton, causing pain and stiffness. Currently, research on ferroptosis is still in its early stages; therefore, exploring the pathogenesis of ferroptosis and its role in various diseases, and proposing effective and targeted treatment methods have significant theoretical significance and practical value.