Fgf10, a secreted ligand, is a multifunctional mesenchymal-epithelial signaling growth factor. It acts via the Fibroblast growth factor receptor 2b (Fgfr2b) with heparan sulfate as co-factor, activating intracellular signaling cascades related to cell proliferation, differentiation, and invasion [3]. Fgf10 is essential for multi-organ development, tissue homeostasis in adults, and is involved in various biological processes [3]. Genetic models, such as knockout mice, have been crucial in studying its functions.

In mouse models, Fgf10 knockout leads to severe phenotypes, including complete truncation of the fore-and hindlimbs and death shortly after birth due to impaired lung development, indicating its essential role in lung and limb formation [4]. In adult mice, reduced Fgf10 expression after myocardial infarction (MI) results in impaired cardiomyocyte proliferation, enhanced cardiac fibrosis, worsened cardiac function, and remodelling. Conversely, conditional Fgf10 overexpression post-MI preserves cardiac remodelling and function by enhancing cardiomyocyte proliferation and preventing myofibroblast activation [1]. Exogenous administration of Fgf10 alleviates allergic airway inflammation in asthma mice, potentially through inhibiting the PI3K/AKT/NF-κB pathway [2].

In conclusion, Fgf10 plays essential roles in organ development, tissue homeostasis, and disease processes. Studies using Fgf10 knockout or conditional knockout mouse models have revealed its significance in heart regeneration and repair, as well as in allergic airway inflammation. Understanding Fgf10's functions can provide insights into potential therapeutic targets for related diseases.