This was possibly due to the protection of mitochondria in stressed HK-2 cells by TFAM-induced mtDNA maintenance.40 Additionally, it was discovered that mitochondria-located circular RNA (circRNA) and steatohepatitis-associated circRNA ATP5B regulator (circRNA SCAR) could reduce ROS production and avoid fibroblast activation via mitochondrial permeability transition during NAFLD.429 Through binding with ATP5B of the mPTP complex, the circRNA SCAR could block cyclophilin D-mPTP interactions, thereby inhibiting the opening of mPTP and reducing ROS production. This evidence concerns the gene ATP5F1B and metabolic dysfunction-associated steatotic liver disease.