<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>5(6)</volume><submitter>Ji X</submitter><pubmed_abstract>The role of ambient air pollution is considered to be important in the development of chronic obstructive pulmonary disease (COPD), and pulmonary hypertension (PH) is a common clinical manifestation of COPD. However, many studies have mainly focused on the adverse health effects of a single air pollutant, ignoring the combined toxicity of multiple pollutants. In the present study, we co-exposed mice to coal-burning air pollutants (SO&lt;sub>2&lt;/sub>, NO&lt;sub>2&lt;/sub> and PM&lt;sub>2.5&lt;/sub>), and confirmed PH-like injury occurrence by airflow limitation, marked abnormal endothelin-1 (ET-1) and endothelial nitric oxide synthase (eNOS) expression, and histopathological and ultrastructural alteration. Global microRNA (miRNA) arrays identified three significantly changed miRNAs homologous with humans (</pubmed_abstract><journal>Toxicology research</journal><pagination>1548-1560</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6062392</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>MicroRNA-338-5p modulates pulmonary hypertension-like injuries caused by SO&lt;sub>2&lt;/sub>, NO&lt;sub>2&lt;/sub> and PM&lt;sub>2.5&lt;/sub> co-exposure through targeting the HIF-1α/Fhl-1 pathway.</pubmed_title><pmcid>PMC6062392</pmcid><pubmed_authors>Li G</pubmed_authors><pubmed_authors>Ji X</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Yun Y</pubmed_authors><pubmed_authors>Sang N</pubmed_authors><pubmed_authors>Ku T</pubmed_authors></additional><is_claimable>false</is_claimable><name>MicroRNA-338-5p modulates pulmonary hypertension-like injuries caused by SO&lt;sub>2&lt;/sub>, NO&lt;sub>2&lt;/sub> and PM&lt;sub>2.5&lt;/sub> co-exposure through targeting the HIF-1α/Fhl-1 pathway.</name><description>The role of ambient air pollution is considered to be important in the development of chronic obstructive pulmonary disease (COPD), and pulmonary hypertension (PH) is a common clinical manifestation of COPD. However, many studies have mainly focused on the adverse health effects of a single air pollutant, ignoring the combined toxicity of multiple pollutants. In the present study, we co-exposed mice to coal-burning air pollutants (SO&lt;sub>2&lt;/sub>, NO&lt;sub>2&lt;/sub> and PM&lt;sub>2.5&lt;/sub>), and confirmed PH-like injury occurrence by airflow limitation, marked abnormal endothelin-1 (ET-1) and endothelial nitric oxide synthase (eNOS) expression, and histopathological and ultrastructural alteration. Global microRNA (miRNA) arrays identified three significantly changed miRNAs homologous with humans (</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Nov</publication><modification>2025-04-04T09:46:40.244Z</modification><creation>2019-03-26T23:50:41Z</creation></dates><accession>S-EPMC6062392</accession><cross_references><pubmed>30090456</pubmed><doi>10.1039/c6tx00257a</doi></cross_references></HashMap>