Liver fibrosis is a sign of non-alcoholic fatty liver disease progression towards steatohepatitis (NASH) and cirrhosis, and aging accelerates this process. Glutaredoxin-1 (Glrx) controls redox signaling by reversing protein S-glutathionylation induced by oxidative stress, and its deletion causes fatty liver in mice. Glrx regulates various pathways, including metabolism and apoptosis, but its regulation of liver fibrosis is unknown. Therefore, we evaluated the role of Glrx in age-induced liver fibrosis and diet-induced NASH in mice. We found that: 1) upregulation of Glrx expression inhibits age-induced hepatic apoptosis and liver fibrosis.