Fgf20, or Fibroblast growth factor 20, is a neurotrophic factor and a member of the FGF9 subfamily. It binds to receptors like FGFR4, FGFR3b, FGFR2b, and FGFRc splice forms. It has a wide-spread expression, playing important roles in embryonic development and in the adult brain. Fgf20 is involved in multiple pathways such as MAPK, PI3K, and β-catenin-related signaling, which are crucial for various biological processes [1,2,3].

Fgf20 mouse mutants display diverse phenotypes. They have congenital deafness, lack of hair, small kidneys, and delayed mammary ductal outgrowth, highlighting its significance in inner ear, hair, kidney, and mammary gland development [1]. In cochlear development, FGF20-FGFR1 signaling through MAPK and PI3K controls sensory progenitor differentiation [3]. In glioma, glioma-cell-derived FGF20 acts on macrophages, suppressing their pro-inflammatory phenotype via β-catenin activation [2]. In ulcerative colitis mouse models, overexpression of FGF20 alleviates symptoms by modulating gut microbiota [4]. Also, in traumatic brain injury and spinal cord injury mouse models, FGF20 shows protective effects, such as maintaining blood-brain barrier integrity and promoting spinal cord injury repair [5,6].

In conclusion, Fgf20 is essential for multiple biological processes, as revealed by mouse models. It plays a role in embryonic development, tissue homeostasis, and the regulation of immune-related functions. Mouse models of Fgf20 knockout or overexpression have provided insights into its functions in diseases like Parkinson's disease, cancer, hereditary deafness, and inflammatory bowel disease, offering potential directions for therapeutic strategies [1,2,4,7].