Abstract

Ferroptosis is a type of nonapoptotic regulated cell death (RCD) manifesting as changes in the regulatory signaling of multiple organelles. Currently, part of the upstream execution mechanism of ferroptosis, namely, the production of unstable iron pools and/or the inhibition or inactivation of glutathione peroxidase 4 (GPX4), and the downstream trigger mechanism of lipid peroxide production and accumulation have been clarified. In addition, ferroptosis-related signaling molecules can undergo protein posttranslational modification to enable their participation in the regulation of signaling network functions. Our understanding of ferroptosis is based on observations of invertebrates and mammals. Although the ferroptosis mechanism in aquatic organisms and terrestrial organisms has been well conserved throughout evolution, some components of the ferroptosis pathway differ. As a newly discovered type of cell death, ferroptosis may be at the root of many diseases. Given that aquatic animal diseases present major challenges to the development of aquaculture, interest in ferroptosis has increased dramatically in recent years, and reports of iron-based programmed death of fish cells will continue to strengthen. Ferroptosis in fish can be mediated by human intervention, thereby providing a possible breakthrough for inhibiting disease processes and improving fish health.

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