TRIM26 deficiency promotes liver fibrosis progression by mediating macrophage polarization via the EZH2-STAT1 axis

Key Points

• Liver fibrosis progression is enhanced with trim26 deficiency, leading to altered macrophage polarization and inflammation.
• Key evidence shows a significant increase in fibrosis markers in trim26-deficient models, indicating the role of ezh2-stat1 pathways.
• Analysis reveals that trim26 interacts with ezh2 and stat1, mediating macrophage responses in liver fibrosis progression.
• This work highlights the potential for targeting trim26 pathways to prevent liver fibrosis, warranting further investigation into therapeutic applications.