Ferroptosis is a kind of regulated cell death (RCD) caused by the redox state disorder of intracellular microenvironment controlled by
glutathione (GSH)
peroxidase 4 (GPX4), which is inhibited by
iron chelators and lipophilic
antioxidants. In addition to classical regulatory mechanisms, new regulatory factors for ferroptosis have been discovered in recent years, such as the P53 pathway, the activating
transcription factor (ATF)3/4 pathway,
Beclin 1 (BECN1) pathway, and some
non-coding RNA. Ferroptosis is closely related to
cancer treatment,
neurodegenerative diseases,
ischemia-reperfusion of organ, neurotoxicity, and others, in particular, in the field of
neurodegenerative diseases treatment has aroused people's interest. The
nuclear factor E2 related factor 2 (Nrf2/NFE2L2) has been proved to play a key role in
neurodegenerative disease treatment and ferroptosis regulation. Ferroptosis promotes the progression of
neurodegenerative diseases, while the expression of Nrf2 and its target genes (Ho-1, Nqo-1, and Trx) has been declined with aging; therefore, there is still insufficient evidence for ferroptosis and Nrf2 regulatory networks in the field of
neurodegenerative diseases. In this review, we will provide a brief overview of ferroptosis regulatory mechanisms, as well as an emphasis on the mechanism of Nrf2 regulating ferroptosis. We also highlight the role of ferroptosis and Nrf2 during the process of
neurodegenerative diseases and investigate a theoretical basis for further research on the relationship between Nrf2 and ferroptosis in the process of
neurodegenerative diseases treatment.