<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>17(11)</volume><submitter>Jin J</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Cigarette smoke extract (CSE) induces reactive oxygen species (ROS) generation in human bronchial epithelial cells, leading to mitochondrial dysfunction and subsequently triggering the mitochondrial unfolded protein response (UPR&lt;sup>mt&lt;/sup>) mediated by the bZIP transcription factor activating transcription factor 4 (ATF-4). This study aimed to investigate whether UPR&lt;sup>mt&lt;/sup> and ATF-4 are involved in the pathway of mitochondrial function impairment in BEAS-2B cells caused by CSE.&lt;h4>Methods&lt;/h4>BEAS-2B bronchial epithelial cells were treated with different concentrations of CSE, and mitochondrial function was detected by JC-1 staining and MitoSoxRed staining. The expression and localisation of translocase of inner mitochondrial membrane 23 (Tim23) and ATF-4 were </pubmed_abstract><journal>Journal of thoracic disease</journal><pagination>9586-9597</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12688523</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Involvement of mitochondrial unfolded protein response and activating transcription factor 4 in the mitochondrial damage pathway of BEAS-2B cells induced by cigarette smoke extracts.</pubmed_title><pmcid>PMC12688523</pmcid><pubmed_authors>Wang S</pubmed_authors><pubmed_authors>Huang M</pubmed_authors><pubmed_authors>Ma H</pubmed_authors><pubmed_authors>Xu F</pubmed_authors><pubmed_authors>Lv D</pubmed_authors><pubmed_authors>Ding Q</pubmed_authors><pubmed_authors>Jin J</pubmed_authors><pubmed_authors>Fu P</pubmed_authors><pubmed_authors>Cen T</pubmed_authors><pubmed_authors>Fei L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Involvement of mitochondrial unfolded protein response and activating transcription factor 4 in the mitochondrial damage pathway of BEAS-2B cells induced by cigarette smoke extracts.</name><description>&lt;h4>Background&lt;/h4>Cigarette smoke extract (CSE) induces reactive oxygen species (ROS) generation in human bronchial epithelial cells, leading to mitochondrial dysfunction and subsequently triggering the mitochondrial unfolded protein response (UPR&lt;sup>mt&lt;/sup>) mediated by the bZIP transcription factor activating transcription factor 4 (ATF-4). This study aimed to investigate whether UPR&lt;sup>mt&lt;/sup> and ATF-4 are involved in the pathway of mitochondrial function impairment in BEAS-2B cells caused by CSE.&lt;h4>Methods&lt;/h4>BEAS-2B bronchial epithelial cells were treated with different concentrations of CSE, and mitochondrial function was detected by JC-1 staining and MitoSoxRed staining. The expression and localisation of translocase of inner mitochondrial membrane 23 (Tim23) and ATF-4 were </description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Nov</publication><modification>2026-06-06T00:33:57.023Z</modification><creation>2026-05-24T03:11:56.181Z</creation></dates><accession>S-EPMC12688523</accession><cross_references><pubmed>41376971</pubmed><doi>10.21037/jtd-2025-460</doi></cross_references></HashMap>