Ferroptosis is a recently discovered form of iron-dependent, non-apoptotic cell death characterized by the accumulation of lipid reactive oxygen species (ROS) and iron. Recent studies have shown that ferroptosis is closely associated with various diseases, including tumors, neurological disorders, ischemia-reperfusion injury, kidney injury, and blood disorders. The occurrence of ferroptosis is influenced by factors that affect glutathione peroxidase (GPX4) activity, leading to a decrease in antioxidant capacity and an accumulation of lipid ROS, ultimately causing oxidative cell death. This paper provides a comprehensive overview of the latest advancements in ferroptosis research, highlighting its pathogenesis and potential therapeutic targets. Key mechanisms of ferroptosis include the suppression of system Xc-, inhibition of GPX4 activity, mitochondrial dysfunction, and the role of P53. Additionally, the paper discusses the involvement of ferroptosis in various diseases, such as pancreatic cancer, hepatocellular carcinoma, gastric cancer, colorectal cancer, breast cancer, lung cancer, clear cell renal cell carcinoma, adrenocortical carcinomas, ovarian cancer, melanoma, head and neck cancer, neurodegenerative disorders, stroke, traumatic brain injury, acute kidney injury, and ischemia-reperfusion injury. The relationship between ferroptosis and other types of cell death, as well as the role of iron and other metal ions in ferroptosis, are also explored. Despite the progress, many aspects of ferroptosis, such as its integration with other cell death modes and the specific molecular mechanisms, remain to be fully understood.Ferroptosis is a recently discovered form of iron-dependent, non-apoptotic cell death characterized by the accumulation of lipid reactive oxygen species (ROS) and iron. Recent studies have shown that ferroptosis is closely associated with various diseases, including tumors, neurological disorders, ischemia-reperfusion injury, kidney injury, and blood disorders. The occurrence of ferroptosis is influenced by factors that affect glutathione peroxidase (GPX4) activity, leading to a decrease in antioxidant capacity and an accumulation of lipid ROS, ultimately causing oxidative cell death. This paper provides a comprehensive overview of the latest advancements in ferroptosis research, highlighting its pathogenesis and potential therapeutic targets. Key mechanisms of ferroptosis include the suppression of system Xc-, inhibition of GPX4 activity, mitochondrial dysfunction, and the role of P53. Additionally, the paper discusses the involvement of ferroptosis in various diseases, such as pancreatic cancer, hepatocellular carcinoma, gastric cancer, colorectal cancer, breast cancer, lung cancer, clear cell renal cell carcinoma, adrenocortical carcinomas, ovarian cancer, melanoma, head and neck cancer, neurodegenerative disorders, stroke, traumatic brain injury, acute kidney injury, and ischemia-reperfusion injury. The relationship between ferroptosis and other types of cell death, as well as the role of iron and other metal ions in ferroptosis, are also explored. Despite the progress, many aspects of ferroptosis, such as its integration with other cell death modes and the specific molecular mechanisms, remain to be fully understood.