Background/Objectives: Ferroptosis is a regulated form of cell death that occurs in the state of oxidative–antioxidative imbalance of an organism. The main components of ferroptosis are lipid peroxidation and iron accumulation. Cells experiencing ferroptosis show swelling, shrunken mitochondria with an abnormal structure, atrophic cristae, dense mitochondrial membranes, and ruptured outer membrane. Ferroptotic cells demonstrate a normal nucleus size without nuclear concentration, and neither condensation nor chromatin margination. Ferroptosis is regulated by multiple protein, genetic, and metabolic factors. The aim of this article is to present ferroptosis as a model of cell death occurring in various conditions and diseases. Methods: A literature search of PubMed, Web of Science was performed. Search terms included “ferroptosis”, “lipid peroxidation”, “iron”, and “cell death”. Results: Ferroptosis affects the onset, course, progression, and treatment of diseases, including neurodegenerative diseases, cancer diseases, autoimmune diseases, and hemorrhages. By using appropriate ferroptosis moderators, it is possible to influence the course of the disease in patients. Conclusions: By understanding the ferroptosis phenomenon well, it is possible to regulate its occurrence by considering the action of oxidative and antioxidant factors. A comprehensive understanding of ferroptosis and the factors regulating this process should be the goal in therapy for many diseases.
Kielan et al. (Mon,) studied this question.