<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>25(1)</volume><submitter>Yao LP</submitter><pubmed_abstract>Chronic obstructive pulmonary disease (COPD) is an irreversible and progressive chronic inflammatory lung disease which affects millions of people worldwide. Activated fibroblasts are observed to accumulate in lung of COPD patients and promote COPD progression through aberrant extracellular matrix (ECM) deposition. In this study, we identified that miR-1307-5p expression was significantly increased in lung fibroblasts derived from COPD patients. Mechanistically, we found that upregulation of miR-1307-5p promoted TGF-β induced lung fibroblast activation and transdifferentiation. We also identified FBXL16 as a direct target for miR-1307-5p mediated myofibroblast activation in COPD. Knockdown of FBXL16 by siRNA prominently increased the expression of myofibroblast markers in MRC-5 fibroblasts</pubmed_abstract><journal>Respiratory research</journal><pagination>376</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11488235</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>MiR-1307-5p enhances fibroblast transdifferentiation to exacerbate chronic obstructive pulmonary disease through regulating FBXL16/HIF1α axis.</pubmed_title><pmcid>PMC11488235</pmcid><pubmed_authors>Zhang F</pubmed_authors><pubmed_authors>Qian MX</pubmed_authors><pubmed_authors>Zheng Q</pubmed_authors><pubmed_authors>Lu F</pubmed_authors><pubmed_authors>Hua ZD</pubmed_authors><pubmed_authors>Wang ZK</pubmed_authors><pubmed_authors>Zhu SM</pubmed_authors><pubmed_authors>Xu LF</pubmed_authors><pubmed_authors>Chen SJ</pubmed_authors><pubmed_authors>Yao LP</pubmed_authors><pubmed_authors>Jiang XQ</pubmed_authors><pubmed_authors>Jiang B</pubmed_authors><pubmed_authors>Chen CS</pubmed_authors><pubmed_authors>Gao DD</pubmed_authors></additional><is_claimable>false</is_claimable><name>MiR-1307-5p enhances fibroblast transdifferentiation to exacerbate chronic obstructive pulmonary disease through regulating FBXL16/HIF1α axis.</name><description>Chronic obstructive pulmonary disease (COPD) is an irreversible and progressive chronic inflammatory lung disease which affects millions of people worldwide. Activated fibroblasts are observed to accumulate in lung of COPD patients and promote COPD progression through aberrant extracellular matrix (ECM) deposition. In this study, we identified that miR-1307-5p expression was significantly increased in lung fibroblasts derived from COPD patients. Mechanistically, we found that upregulation of miR-1307-5p promoted TGF-β induced lung fibroblast activation and transdifferentiation. We also identified FBXL16 as a direct target for miR-1307-5p mediated myofibroblast activation in COPD. Knockdown of FBXL16 by siRNA prominently increased the expression of myofibroblast markers in MRC-5 fibroblasts</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Oct</publication><modification>2026-07-14T20:44:07.825Z</modification><creation>2025-04-04T20:55:39.615Z</creation></dates><accession>S-EPMC11488235</accession><cross_references><pubmed>39420370</pubmed><doi>10.1186/s12931-024-03007-6</doi></cross_references></HashMap>