{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE315nnn/GSE315897/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE315897"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Loss of the Mitochondrial Regulator TFAM in Alveolar Epithelial Cells Drives Lung Fibrosis [in vitro]","description":"Mitochondrial dysfunction in alveolar epithelial cells is implicated in idiopathic pulmonary fibrosis (IPF), but the upstream epithelial drivers remain unclear. This study tests whether loss of TFAM, a key regulator of mitochondrial DNA maintenance and oxidative phosphorylation, is sufficient to reprogram alveolar type 2 (AT2) cells and promote pro-fibrotic gene programs. We generated bulk RNA-seq datasets from (i) primary mouse AT2 cells following ex vivo Cre-mediated Tfam deletion versus matched controls and (ii) whole-lung tissue from mice with AT2-specific Tfam loss versus controls. These data enable analysis of TFAM-dependent epithelial stress and state-transition signatures and associated remodeling pathways.","dates":{"publication":"2026/09/22"},"accession":"GSE315897","cross_references":{"GSM":["GSM9439421","GSM9439420","GSM9439423","GSM9439422","GSM9439425","GSM9439424","GSM9439418","GSM9439419"],"GPL":["24247"],"GSE":["315897"],"taxon":["Mus musculus"],"PMID":["[42523419]"]}}