AKR1C3 promotes aerobic glycolysis in hepatic stellate cells via the AKT/mTOR pathway to induce liver fibrosis

Key Points

• Aerobic glycolysis is significantly enhanced, leading to increased liver fibrosis.
• Inhibition of the AKT/mTOR pathway may reduce fibrosis progression in targeted cell types.
• Mechanisms include enhanced cellular metabolism and growth signaling pathways in liver cells.
• Findings underscore the potential for targeting AKR1C3 in liver disease therapies.