{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["10(1)"],"submitter":["Kim S"],"pubmed_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"],"journal":["Signal transduction and targeted therapy"],"pagination":["322"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12489044"],"repository":["biostudies-literature"],"pubmed_title":["Colony-stimulating factor 3 as a key mediator in the progression of idiopathic pulmonary fibrosis: a novel therapeutic target."],"pmcid":["PMC12489044"],"pubmed_authors":["Kim TS","Yi JM","Lee SJ","Choi HS","Lee ES","Jin YW","Kim S","Lee EJ","Song JW","Kang JH","Kim Y","Kim MJ","Yun IY","Kim RK"],"additional_accession":[]},"is_claimable":false,"name":"Colony-stimulating factor 3 as a key mediator in the progression of idiopathic pulmonary fibrosis: a novel therapeutic target.","description":"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","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Oct","modification":"2026-06-04T01:54:07.387Z","creation":"2026-05-04T03:14:08.319Z"},"accession":"S-EPMC12489044","cross_references":{"pubmed":["41034234"],"doi":["10.1038/s41392-025-02421-6"]}}