Blocking ATP1V6G3 triggers liver support cell aging and reduces scar tissue through Notch1 pathway to ease liver fibrosis

Preliminary results show upregulation of ATP6V1G3 in human fibrotic livers and murine liver fibrosis models.

• Activated hepatic stellate cells (aHSCs) contribute to liver fibrosis through excessive accumulation of extracellular matrix (ECM).
• Senescence of aHSCs is linked to the degradation of ECM and potential regression of hepatic fibrosis.
• Inhibition of ATP6V1G3 triggered senescence in aHSCs during in vitro experiments.
• Blocking Notch1 signaling reversed the senescence effects induced by ATP6V1G3 inhibition.
• Targeting ATP6V1G3 may provide a new therapeutic approach for managing hepatic fibrosis.

Simplified