Fzd6, a member of the Frizzled family of G protein-coupled receptors, is a key mediator in Wnt signaling pathways. Wnt ligands bind to Fzd6, along with co-receptors like Lrp5/6, to initiate either canonical or non-canonical Wnt signaling, which play fundamental roles in cell differentiation, tissue polarity during development, and stem cell specification and activity [1,2,3].

In lung alveoli, Fzd6 is expressed in epithelial cells and, unexpectedly, activation of non-canonical Fzd6 can stimulate alveolar epithelial stem cell activity and promote an alveolar fate in airway-derived progenitors, offering a potential lung injury regeneration strategy [1].

In melanoma, knockout of Fzd6 significantly reduces cell invasion and lung metastasis, revealing its role in melanoma progression via regulating canonical Wnt signaling and epithelial-mesenchymal transition [2].

In osteoporotic mice, Fzd6 silencing down-regulates the osteogenic ability of adipose-derived stem cells both in vitro and in vivo, indicating its importance in regulating osteogenic differentiation [4].

In conclusion, Fzd6 is crucial for multiple biological processes through its involvement in Wnt signaling. Studies using gene knockout mouse models have revealed its roles in lung injury regeneration, melanoma progression, and osteogenic differentiation, providing insights into potential therapeutic strategies for related diseases.