PPARGC1A and metabolic dysfunction-associated steatohepatitis: By generating mice with hepatic-specific overexpressed PGC-1α, we show here that in comparison to that of WT mice, a mild PGC-1α elevation in the liver is sufficient to ameliorate nonalcoholic steatohepatitis phenotype of hepatic inflammation, fibrosis, and oxidative stress by enhanced mitochondrial function and fatty acid oxidation in mice fed with MCD.