Arid1a loss drives non-alcoholic steatohepatitis in mice via epigenetic dysregulation of hepatic lipogenesis and fatty acid oxidation

ARID1A, a DNA-binding component of the SWI/SNF ATP-dependent chromatin-remodeling complex, contributes to nucleosome repositioning and access by transcriptional regulators. Liver-specific deletion of Arid1a (Arid1a LKO) caused the development of age-dependent fatty liver disease in mice. Transcriptome analysis revealed upregulation of lipogenesis and down-regulation of fatty acid oxidation genes. Overall design: Livers of P90-day-old mice were collected, and transcriptomic analysis performed via RNA-seq.