GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE315nnn/GSE315898/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE315898GEOGSEfalseLoss of the Mitochondrial Regulator TFAM in Alveolar Epithelial Cells Drives Lung Fibrosis [whole lung]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.2026/09/22GSE315898GSM9439432GSM9439431GSM9439433GSM9439427GSM9439426GSM9439429GSM9439428GSM943943024247315898Mus musculus[42523419]