Abstract: Ferroptosis is an iron-dependent, regulatory form of cell death driven primarily by lipid peroxidation, and it is distinct from apoptosis, necrosis, and pyroptosis in terms of morphology, regulatory mechanisms, biochemistry, and genetics. Over the past decade, studies have shown that ferroptosis, as a key hub linking intracellular iron metabolism, amino acid metabolism, lipid metabolism, and glucose metabolism, is widely involved in the clinical and pathological processes of neurodegenerative diseases(such as Alzheimers disease, Parkinsons disease, and amyotrophic lateral sclerosis)and multi-organ injury(ischemia-reperfusion injury, liver injury, kidney injury, and cardiac injury). This article systematically reviews the core regulatory network of ferroptosis-iron metabolism disorders, imbalance of the antioxidant defense system, and the lipid peroxidation cascade-and focuses on its pathological significance in the central nervous system and multiple peripheral organ injuries. On this basis, it systematically reviews the current status of ferroptosis inducers and inhibitors in clinical development, and further analyzes the challenges faced in targeting ferroptosis for intervention in related diseases, including cell-type specificity, tissue specificity, and drug stability and safety. It also further discusses the application prospects of gene therapy technologies and precise drug delivery systems in the treatment of ferroptosis-related diseases.

Key words: Ferroptosis, Neurodegenerative diseases, Multiple organ injury, Targeted intervention