ABSTRACT
Ferroptosis is a newly discovered non-apoptotic regulatory form of cell death characterized by accumulation of iron-dependent lipid peroxides and reactive oxygen species （ROS）. p53 is a tumor suppressor gene that can induce cell cycle arrest， apoptosis， autophagy， and senescence to maintain genomic stability by mediating transcriptional regulation of a variety of key cellular genes. Recent studies have found that p53 can also regulate ferroptosis bidirectionally by multiple cellular responses including iron metabolism， polyunsaturated fatty acid （PUFAs） metabolism， amino acid metabolism and nicotinamide adenine dinucleotide phosphate （NADPH）-mediated metabolisms， and participate in the pathological progression of diseases such as tumors， nervous system diseases， cardiovascular diseases， liver disease， and kidney disease. This paper provided a systematic review of the mechanism of p53-mediated ferroptosis in the outcome of related diseases and its influencing factors. And the research advance in the mechanisms of targeted regulation of p53-mediated ferroptosis in the prevention and treatment of cancer， stroke， acute ischemic cardiomyopathy， chronic heart failure， atherosclerosis， ulcerative colitis， and adjuvant arthritis by traditional Chinese medicine was also elaborated. This paper was expected to provide new ideas for the prevention and treatment against related diseases.