{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE315nnn/GSE315898/"]},"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=GSE315898"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Loss of the Mitochondrial Regulator TFAM in Alveolar Epithelial Cells Drives Lung Fibrosis [whole lung]","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":"GSE315898","cross_references":{"GSM":["GSM9439432","GSM9439431","GSM9439433","GSM9439427","GSM9439426","GSM9439429","GSM9439428","GSM9439430"],"GPL":["24247"],"GSE":["315898"],"taxon":["Mus musculus"],"PMID":["[42523419]"]}}