Fmo2, or flavin-containing monooxygenase 2, is involved in multiple biological processes and disease-related pathways. It has been shown to play roles in processes such as lipogenesis regulation, immune-related responses, and cell protection mechanisms. Genetic models, like gene knockout (KO) and conditional knockout (CKO) mouse models, have been crucial for studying its functions [1,3,5].

In the context of 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. In contrast, FMO2 overexpression improved NAFL/NASH. 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 [1].

In epithelial ovarian cancer, FMO2 is upregulated in tumor stroma, correlates with fibroblast activation, and predicts a worse clinical outcome. It also contributes to immune cell infiltration, especially of CD163 + macrophages [2].

In the heart, genetic deletion of FMO2 in cardiomyocytes reduced cell survival and enhanced cardiac dysfunction after ischemic injury, while cardiomyocyte-specific overexpression had a protective effect. FMO2 inhibits ER stress-induced apoptotic proteins through its disulfide bond catalytic activity [3].

In breast cancer, FMO2 is downregulated and is closely related to clinical indicators. Decreased FMO2 expression is associated with poor survival, and it may be related to immunotherapy sensitivity [4].

In post-myocardial infarction cardiac remodeling, CELF1 promotes remodeling by suppressing FMO2, and FMO2 overexpression can improve extracellular matrix deposition and cardiac remodeling [5].

In lung adenocarcinoma, circ_MACF1 upregulates FMO2 by targeting miR-421, suppressing paclitaxel resistance and malignant cellular behaviors [6].

In conclusion, Fmo2 plays essential roles in various biological processes and disease conditions. Studies using KO/CKO mouse models have revealed its significance in diseases such as NAFLD, epithelial ovarian cancer, ischemic heart disease, breast cancer, post-myocardial infarction cardiac remodeling, and lung adenocarcinoma. Understanding Fmo2 functions provides insights into disease mechanisms and potential therapeutic targets.