Csf3, also known as colony-stimulating factor 3 or G-CSF, is a key cytokine in neutrophil production and function. It stimulates the maturation, proliferation, and trafficking of myeloid progenitor cells, and is involved in cytokine-cytokine receptor interaction pathways. It plays a crucial role in maintaining normal immune function related to neutrophils [1,3].

In humans, biallelic inactivating variants in CSF3 have been found to cause a novel autosomal recessive form of severe congenital neutropenia (SCN), mirroring the phenotype observed in mouse and zebrafish models of CSF3 deficiency [1]. In a mouse model of acute exacerbation of pulmonary fibrosis (AE-PF), exogenous administration of CSF3 protein exacerbated the condition. CSF3 disrupted alveolar epithelial barrier integrity via the PI3K/p-Akt/Snail pathway [2]. In glioma, upregulation of IGF2BP3 enhances E3 ubiquitin protein ligase MIB1 expression, promoting FTO degradation and increasing m6A-mediated CSF3 release and NET formation [4].

In conclusion, CSF3 is essential for neutrophil-related functions. Gene knockout models in mice and other species have revealed its role in diseases such as SCN and AE-PF. Understanding CSF3's functions through these models provides insights into the pathophysiology of related diseases and potential therapeutic targets.