{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["17(11)"],"submitter":["Jin J"],"pubmed_abstract":["<h4>Background</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<sup>mt</sup>) mediated by the bZIP transcription factor activating transcription factor 4 (ATF-4). This study aimed to investigate whether UPR<sup>mt</sup> and ATF-4 are involved in the pathway of mitochondrial function impairment in BEAS-2B cells caused by CSE.<h4>Methods</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 "],"journal":["Journal of thoracic disease"],"pagination":["9586-9597"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12688523"],"repository":["biostudies-literature"],"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."],"pmcid":["PMC12688523"],"pubmed_authors":["Wang S","Huang M","Ma H","Xu F","Lv D","Ding Q","Jin J","Fu P","Cen T","Fei L"],"additional_accession":[]},"is_claimable":false,"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.","description":"<h4>Background</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<sup>mt</sup>) mediated by the bZIP transcription factor activating transcription factor 4 (ATF-4). This study aimed to investigate whether UPR<sup>mt</sup> and ATF-4 are involved in the pathway of mitochondrial function impairment in BEAS-2B cells caused by CSE.<h4>Methods</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 ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Nov","modification":"2026-06-06T00:33:57.023Z","creation":"2026-05-24T03:11:56.181Z"},"accession":"S-EPMC12688523","cross_references":{"pubmed":["41376971"],"doi":["10.21037/jtd-2025-460"]}}