Ferroptosis and the bidirectional regulatory factor p53

Ferroptosis is a type of regulated cell death characterized by iron-mediated lipid peroxidation, in contrast with apoptosis, autophagy, and necrosis. It can be triggered by many pathological processes, including cellular metabolism, tumors, neurodegenerative diseases, cardiovascular diseases, and ischemia-reperfusion injuries. In recent years, ferroptosis has been discovered to be associated with p53. P53 is a tumor suppressor protein with multiple and powerful functions in cell cycle arrest, senescence, cell death, repair of DNA damage, and mitophagy. Emerging evidence shows that ferroptosis plays a crucial role in tumor suppression by p53. P53 functions as a key bidirectional regulator of ferroptosis by adjusting metabolism of iron, lipids, glutathione peroxidase 4, reactive oxygen species, and amino acids via a canonical pathway. In addition, a noncanonical pathway of p53 that regulates ferroptosis has been discovered in recent years. The specific details require to be further clarified. These mechanisms provide new ideas for clinical applications, and translational studies of ferroptosis have been performed to treat various diseases.

Automated summary

Ferroptosis is a regulated cell death caused by iron-mediated lipid peroxidation. It has been found to be associated with p53, a tumor suppressor protein with multiple functions. P53 acts as a bidirectional regulator of ferroptosis by controlling the metabolism of iron, lipids, glutathione peroxidase 4, reactive oxygen species, and amino acids. A noncanonical pathway of p53 that regulates ferroptosis has also been discovered. These mechanisms have potential clinical applications for treating various diseases.