Fmo2, or flavin-containing monooxygenase 2, is involved in multiple biological processes. It may function as a regulator in lipid metabolism-related pathways, as well as in cellular stress response pathways. Its role in maintaining normal physiological functions and its potential in disease-related research make it an important gene for study, and genetic models like knockout mice are valuable tools in understanding its functions [1,2,3].

In non-alcoholic fatty liver disease (NAFLD), both global and hepatocyte-specific knockout of Fmo2 in mice led to increased lipogenesis, severe hepatic steatosis, inflammation, and fibrosis. Mechanistically, FMO2 directly interacts with SREBP1, inhibiting its translocation from the endoplasmic reticulum to the Golgi apparatus and subsequent activation, thus suppressing de novo lipogenesis and improving NAFL/NASH [1]. In the context of myocardial infarction, genetic deletion of Fmo2 in cardiomyocytes resulted in reduced cell survival and enhanced cardiac dysfunction, while cardiomyocyte-specific overexpression had a protective effect. FMO2 inhibited the activation of ER stress-induced apoptotic proteins through down-regulating the unfolded protein response pathway [2]. Also, in post-myocardial infarction cardiac remodeling, CELF1 promoted remodeling by suppressing Fmo2, and Fmo2 overexpression improved extracellular matrix deposition and cardiac remodeling in MI mice [3].

In conclusion, Fmo2 plays crucial roles in lipid metabolism in the liver as well as in protecting cardiomyocytes from ischemic injury and post-myocardial infarction cardiac remodeling. Gene knockout mouse models have been instrumental in revealing these functions, highlighting Fmo2 as a potential target for treating NAFLD and ischemic heart-related diseases.