<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>20(1)</volume><submitter>Yang S</submitter><pubmed_abstract>Chronic exposure to silica can lead to silicosis, one of the most serious occupational lung diseases worldwide, for which there is a lack of effective therapeutic drugs and tools. Epithelial mesenchymal transition plays an important role in several diseases; however, data on the specific mechanisms in silicosis models are scarce. We elucidated the pathogenesis of pulmonary fibrosis via single-cell transcriptome sequencing and constructed an experimental silicosis mouse model to explore the specific molecular mechanisms affecting epithelial mesenchymal transition at the single-cell level. Notably, as silicosis progressed, glycoprotein non-metastatic melanoma protein B (GPNMB) exerted a sustained amplification effect on alveolar type II epithelial cells, inducing epithelial-to-mesenchymal tr</pubmed_abstract><journal>Particle and fibre toxicology</journal><pagination>29</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10354944</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Single-cell transcriptome sequencing-based analysis: probing the mechanisms of glycoprotein NMB regulation of epithelial cells involved in silicosis.</pubmed_title><pmcid>PMC10354944</pmcid><pubmed_authors>Yang L</pubmed_authors><pubmed_authors>Jiang W</pubmed_authors><pubmed_authors>Chao J</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Luo W</pubmed_authors><pubmed_authors>Long M</pubmed_authors><pubmed_authors>Yuan M</pubmed_authors><pubmed_authors>Yang S</pubmed_authors><pubmed_authors>Sun Y</pubmed_authors><pubmed_authors>Zhou X</pubmed_authors><pubmed_authors>Cheng Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Single-cell transcriptome sequencing-based analysis: probing the mechanisms of glycoprotein NMB regulation of epithelial cells involved in silicosis.</name><description>Chronic exposure to silica can lead to silicosis, one of the most serious occupational lung diseases worldwide, for which there is a lack of effective therapeutic drugs and tools. Epithelial mesenchymal transition plays an important role in several diseases; however, data on the specific mechanisms in silicosis models are scarce. We elucidated the pathogenesis of pulmonary fibrosis via single-cell transcriptome sequencing and constructed an experimental silicosis mouse model to explore the specific molecular mechanisms affecting epithelial mesenchymal transition at the single-cell level. Notably, as silicosis progressed, glycoprotein non-metastatic melanoma protein B (GPNMB) exerted a sustained amplification effect on alveolar type II epithelial cells, inducing epithelial-to-mesenchymal tr</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jul</publication><modification>2025-04-26T11:31:09.734Z</modification><creation>2024-12-04T01:36:32.136Z</creation></dates><accession>S-EPMC10354944</accession><cross_references><pubmed>37468937</pubmed><doi>10.1186/s12989-023-00543-9</doi></cross_references></HashMap>