Colony-stimulating factor 3 as a key mediator in the progression of idiopathic pulmonary fibrosis: a novel therapeutic target.

ABSTRACT: Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease characterized by excessive ECM deposition and myofibroblast accumulation driven by cytokine dysregulation. This study identified granulocyte colony-stimulating factor 3 (CSF3) as a key mediator of IPF progression. Elevated CSF3 expression was observed in the lung tissues of IPF patients. Recombinant CSF3 promoted myofibrogenesis in lung fibroblasts, whereas CSF3-deficient mice were protected from bleomycin-induced pulmonary fibrosis. Treatment with novel CSF3-neutralizing antibodies significantly restored fibrosis in IPF mice by suppressing myofibroblast differentiation and reducing ECM deposition. Here, we demonstrated a reciprocal regulatory relationship between CSF3 and TGF-β that amplifies pro-fibrotic signaling. Our mechanist

SUBMITTER: Kim S 

PROVIDER: S-EPMC12489044 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature