Cell Death Dis: PGC-1 alpha low expression exacerbates hepatic cell epithelial-interstitial transformation and liver fibrosis

Liver fibrosis occurs in a variety of liver diseases, including hepatitis and chronic alcoholism, and can lead to scarring, resulting in liver damageHepatic fibrosis is a wound healing reaction characterized by excessive protein deposition, liver cell damage, liver leaf distortion and vascular structure changes in extracellular matrix (ECM)If left untreated, liver fibrosis eventually develops into cirrhosis or hepatocellular carcinomamitochondrial dynamics imbalance induced by oxidative stress may lead to the process of epithelial translatlythestion (EMT) in liver cells and liver fibrosis, but its potential molecular mechanisms remain to be studiedresearchers studied the role of mitochondrial dynamics in the process of emtly thoratology and liver fibrosis in human-derived liver cell lineL L-02 cells and mouse models of hepatofibrosisresults showed that mitochondrial DNA damage induced by oxidative stress was associated with abnormal division of mitochondria and emtit in liver cellsReactive oxygen (ROS) effectively weakens abnormal mitochondrial division and liver fibrosis induced by the removal of Apocynin and mitochondrial antioxidant Mito-tempoRestoring mitochondrial biology can weaken the EMT response of liver cellsthe abnormal division of the abnormal division of liver cells induced by oxidative stress mainly involved the reduction of the expression level of PGC-1 alphaCompared with wild type, CCl4 stimulation can further increase the abnormal division of the mitochondria of the PGC-1 alpha gene in mice, making liver fibrosis more severeresults show that PGC-1 alpha has protective effect in oxidative stress-induced hepatocellular EMT and hepatic fibrosis