{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kim JY"],"funding":["Ministry of Science and ICT, South Korea"],"pagination":["140"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11566568"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(1)"],"pubmed_abstract":["<h4>Background</h4>In understanding the pathophysiology of pulmonary fibrosis (PF), macrophage plasticity has been implicated with a crucial role in the fibrogenic process. Growing evidence indicates that accumulation of M2 macrophages correlates with the progression of PF, suggesting that targeted modulation of molecules that influence M2 macrophage polarization could be a promising therapeutic approach for PF. Here, we demonstrated a decisive role of C-X-C motif chemokine ligand 11 (CXCL11) in driving M1 macrophage polarization to alleviate PF in the bleomycin-induced murine model.<h4>Results</h4>We intravenously administered secretome derived from naïve (M0) and polarized macrophages (M1 and M2) into PF mice and found that lung fibrosis was effectively reversed in only the M1-treated gr"],"journal":["Cell & bioscience"],"pubmed_title":["CXCL11 reprograms M2-biased macrophage polarization to alleviate pulmonary fibrosis in mice."],"pmcid":["PMC11566568"],"funding_grant_id":["22A0304L1-01","RS-2023-00212166","2022M3A9E4016936","2022RIS-005"],"pubmed_authors":["Hong IS","Lee SJ","Park M","Cho DW","Song H","Yang SR","Kim WJ","Kim JY","Choi JY","Jeong S","Kang M","Hong SH","Chang H"],"additional_accession":[]},"is_claimable":false,"name":"CXCL11 reprograms M2-biased macrophage polarization to alleviate pulmonary fibrosis in mice.","description":"<h4>Background</h4>In understanding the pathophysiology of pulmonary fibrosis (PF), macrophage plasticity has been implicated with a crucial role in the fibrogenic process. Growing evidence indicates that accumulation of M2 macrophages correlates with the progression of PF, suggesting that targeted modulation of molecules that influence M2 macrophage polarization could be a promising therapeutic approach for PF. Here, we demonstrated a decisive role of C-X-C motif chemokine ligand 11 (CXCL11) in driving M1 macrophage polarization to alleviate PF in the bleomycin-induced murine model.<h4>Results</h4>We intravenously administered secretome derived from naïve (M0) and polarized macrophages (M1 and M2) into PF mice and found that lung fibrosis was effectively reversed in only the M1-treated gr","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Nov","modification":"2025-04-05T13:50:54.526Z","creation":"2025-04-05T13:50:54.526Z"},"accession":"S-EPMC11566568","cross_references":{"pubmed":["39548525"],"doi":["10.1186/s13578-024-01320-7"]}}