Loss of the Mitochondrial Regulator TFAM in Alveolar Epithelial Cells Drives Lung Fibrosis [in vitro]

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.