08 January 2024 | Dongmei Zhou, Peipei Lu, Xianglai Mo, Bing Yang, Ting Chen, You Yao, Tian Xiong, Lin Yue, Xi Yang
This review explores the association between ferroptosis and metabolic syndrome (MetS) and its complications, including obesity, type 2 diabetes (T2DM), and atherosclerosis. Ferroptosis, a novel form of cell death characterized by iron overload, lipid peroxide accumulation, and decreased glutathione peroxidase 4 (GPX4) activity, is linked to various metabolic disorders. The review discusses the mechanisms of ferroptosis, the regulatory roles of inducers and inhibitors, and the significance of iron loading in MetS. It highlights the role of ferroptosis in the pathogenesis of MetS and its complications, such as obesity, T2DM, and atherosclerosis. The review also discusses potential therapeutic strategies targeting ferroptosis, including iron chelators and antioxidants, and presents a list of drugs or small molecules that can alleviate MetS and its complications by targeting ferroptosis. The findings suggest that manipulating intracellular iron levels and inhibiting ferroptosis may be viable approaches to treating MetS and its associated conditions.This review explores the association between ferroptosis and metabolic syndrome (MetS) and its complications, including obesity, type 2 diabetes (T2DM), and atherosclerosis. Ferroptosis, a novel form of cell death characterized by iron overload, lipid peroxide accumulation, and decreased glutathione peroxidase 4 (GPX4) activity, is linked to various metabolic disorders. The review discusses the mechanisms of ferroptosis, the regulatory roles of inducers and inhibitors, and the significance of iron loading in MetS. It highlights the role of ferroptosis in the pathogenesis of MetS and its complications, such as obesity, T2DM, and atherosclerosis. The review also discusses potential therapeutic strategies targeting ferroptosis, including iron chelators and antioxidants, and presents a list of drugs or small molecules that can alleviate MetS and its complications by targeting ferroptosis. The findings suggest that manipulating intracellular iron levels and inhibiting ferroptosis may be viable approaches to treating MetS and its associated conditions.