The role of ferroptosis in fish inflammation

Ferroptosis, as one of cell death modalities, is driven by iron-dependent phospholipid peroxidation and regulated by various cellular metabolic pathways, including iron, amino acid and lipid metabolism, as well as disease-related signalling pathways. Cell survival or death is a critical issue in the inflammatory response. On the one hand, ferroptosis is more immunogenic than apoptosis, and ruptured ferroptotic cells release damage-associated molecular patterns (DAMPs), which can trigger an inflammatory response. On the other hand, various pathogenic bacteria may cause peroxidation of polyunsaturated fatty acids (PUFAs) on the cell membrane, leading to ferroptosis. In fish, the key genes and signalling pathways related to ferroptosis are conserved, but there are still differences among fish species. In recent years, frequent occurrences of fish diseases have posed a considerable challenge to the large-scale aquaculture. The specific precursors for ferroptotic cell death were iron-dependent oxidative stress and lipid peroxidation, which always occur in fish inflammation. This review summarizes recent studies on ferroptosis in fish inflammation, that is, iron-dependent programmed cell death, to address ferroptosis, inflammation and correlations between them in fish. This review may contribute to a better understanding of the underlying mechanisms of ferroptosis and inflammation in fish and provides suggestions for sustainable development and large-scale aquaculture farming.