Hepcidin is a liver-derived peptide hormone that is related to iron balance and immunity in humans. However, its function in Siniperca chuatsi has not been well elucidated. In this study, we analyzed the expression and function of the S. chuatsi hepcidin (Sc-hep) gene. Sc-hep was specifically expressed in the liver and appeared to be one of the most highly expressed genes in the liver. After spleen and kidney necrosis virus (ISKNV) infection and lipopolysaccharide (LPS) and polyinosinic—polycytidylic acid (Poly I:C) stimulation, the expression of Sc-hep in the liver increased by approximately 110, 6500, and 225 times, respectively. After ferrous sulfate (FS) injection, the expression of Sc-hep in the liver increased approximately 520-fold. We found that miR-19c-5p could inhibit Sc-hep expression. Five CpG dinucleotides distributed in the promoter region showed no differential methylation between the liver and the stomach, both presenting high methylation rates. After FS or LPS injection, the expression of three iron balance-related genes (FPN1, TFR1, and FTN) and five immune-related cytokine genes (IL-1β, IL8, TNF-α, TLR22, and SOCS3) significantly changed. These results indicate that Sc-hep participates in the regulation of iron balance and plays an important role in the immune system. Sc-hep increased approximately 52-fold when mandarin fish were domesticated with artificial diets. Sc-hep might be used as a real-time biomarker of mandarin fish liver because its expression markedly varies under different physiological conditions.

The administration of selective serotonin reuptake inhibitors (SSRIs) during pregnancy can increase the odds of congenital heart defects in babies. The present study aims to explore the toxic effects of SSRIs on the cardiac systems and the underlying mechanism. We apply human pluripotent stem cells to establish 2D-monolayer cardiomyocyte and 3D-cardiac organoid models to evaluate the effects of three SSRIs (fluoxetine, paroxetine, and sertraline) on cardiac development. We observe that SSRIs exposure inhibited ATP production and mitochondrial respiration and disrupted mitochondrial homeostasis and sarcomere structure in the differentiating cardiomyocytes, presenting high risks of dysfunction and abnormality of cardiomyocytes. Further analyses in the cardiac organoid model show that SSRIs not only reduce mitochondrial respiration and ATP production, but may also affect cardiac development and angiogenesis. Altogether, our study reveals that SSRIs induce mitochondrial dysfunction and sarcomeric disorganization in cardiomyocytes, implying their potential risk to the cardiac system.