Ferroptosis is a form of oxidative, iron-dependent, non-apoptotic cell death characterized by the accumulation of lipid peroxides and the depletion of glutathione. Ferroptosis plays a significant role in human cancer and is essential in neurological disorders, including neurodegeneration, stroke, and neurotrauma. One of the key challenges in cancer research is how to effectively kill cancer cells while leaving healthy cells intact. Cancer cells often have defects in cell death executioner mechanisms, which is one of the main reasons for therapy resistance. To enable growth, cancer cells exhibit an increased iron demand compared with normal, non-cancer cells. This iron dependency can make cancer cells more vulnerable to iron-catalyzed necrosis, referred to as ferroptosis. It is a newly identified regulated form of cell death, which is thought to play a major role in neurodegenerative diseases. The mechanisms of ferroptosis in several neurological disorders are discussed in detail in this article. It also provides an overview of emerging medications that target ferroptosis in the treatment of neurological disorders. It also highlights the variations and connections between the different cell death pathways implicated in neurological disorders. Clarifying the function of ferroptosis in the brain will help us better understand the mechanisms behind neurological disorders and offer possible strategies for both acute and long-term neurological illness prevention and therapy. Consequently, we provide an overview and brief description of the main pathways involved in ferroptosis in this review, focusing on its regulation and its dual roles as a tumor suppressor and an oncogenic process in various human malignancies. The identification of FDA-approved drugs as ferroptosis inducers has raised high expectations for ferroptosis as a promising new approach to killing therapy-resistant cancers.
Wal et al. (Mon,) studied this question.