Arthritis remains a common and debilitating disease affecting millions of people worldwide. Osteoarthritis (OA) and rheumatoid arthritis (RA) are among the most common forms of this chronic, degenerative disease, which is moving toward precision medicine.

Ferroptosis is a type of cell death caused by iron-dependent lipid peroxidation. In recent years, certain isoforms of glutathione-S-transferases (GSTs) have been identified that may play a key role in regulating ferroptosis. Previous study demonstrated that the NRF2/GSH/GST/RLIP76 and MRP1 axis acts as an independent anti-ferroptosis pathway. Furthermore, this study evaluated the therapeutic potential of mifepristone (RU486) for mitigating acetaminophen (APAP)-induced liver injury in vivo.

Stroke remains a leading cause of death and long-term disability worldwide, with ischemic stroke representing approximately 85% of all stroke cases. Cerebral ischemia-reperfusion (I/R) injury significantly exacerbates neuronal damage through mechanisms such as oxidative stress, ferroptosis, and endoplasmic reticulum stress (ERS).

Introduction: This study aimed to explore the changes in ferroptosis markers and their relationship with fundus lesion severity in chronic kidney disease (CKD). Methods: We enrolled 118 CKD patients and collected clinical, renal function, fundus imaging data, and ferroptosis markers. We performed correlation and regression analyses between renal dysfunction and fundus lesions, and assessed the changes and mediating roles of serum iron (Fe), malondialdehyde (MDA), and reduced glutathione (GSH) in CKD deterioration and retinal damage.