Foxk1, a forkhead/winged helix transcription factor, is involved in regulating various cellular processes such as cell proliferation, differentiation, and metabolism. It is associated with pathways like Wnt/β -catenin, mTORC1, and aerobic glycolysis, and is of great biological importance in development and disease [3,4,6]. Genetic models, especially KO and CKO mouse models, have been crucial for studying its functions.

In KO mouse models, conditional knockout of Foxk1 in preosteoblasts and mature osteoblasts led to decreased bone mass and mechanical strength due to reduced bone formation, as it was found to target the promoter region of glycolytic enzyme genes and regulate aerobic glycolysis in osteoblasts [1]. Hepatocyte-specific deletion of Foxk1 in mice fed a NASH-inducing diet ameliorated hepatic steatosis, inflammation, fibrosis, and tumorigenesis [2]. Cardiomyocyte-specific knockout of Foxk1 impaired neonatal heart regeneration after myocardial infarction injury [5].

In conclusion, Foxk1 plays vital roles in osteoblast metabolism regulation, hepatic lipid metabolism, and cardiogenesis. Its study using KO and CKO mouse models has provided insights into age-related bone loss, non-alcoholic fatty liver disease, and congenital heart disease, highlighting its potential as a therapeutic target in these disease areas.