Abstract
Ferroptosis is a type of iron-dependent cell death that differs from apoptosis, necroptosis, autophagy, and other forms of cell death. It is mainly characterized by the accumulation of intracellular lipid peroxides, redox imbalance, and reduced levels of glutathione and glutathione peroxidase 4. Studies have demonstrated that ferroptosis plays an important regulatory role in the occurrence and development of neurodegenerative diseases, stroke, traumatic brain injury, and ischemia-reperfusion injuries. Multiple mechanisms, such as iron metabolism, ferritinophagy, p53, and p62/Keap1/Nrf2, as well as the combination of FSP1/CoQ/NADPH and hepcidin/FPN-1 can alter the vulnerability to ferroptosis. Nevertheless, there has been limited research on the development and management of ferroptosis in the realm of eye disorders, with most studies focusing on retinal conditions such as age-related macular degeneration and retinitis pigmentosa. This review offers a thorough examination of the disruption of iron homeostasis in eye disorders, investigating the underlying mechanisms. We anticipate that the occurrence of ferroptotic cell death will not only establish a fresh field of study in eye diseases, but also present a promising therapeutic target for treating these diseases.