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Liver fibrosis remains the critical bottleneck in the progression from chronic liver injury to cirrhosis and hepatocellular carcinoma (HCC). Activated hepatic stellate cells (HSCs) play a central role in this process by secreting excessive extracellular matrix leading to liver scarring, distortion of liver architecture and liver dysfunction.1 Despite intensive efforts to target HSCs and reverse fibrosis, no treatment has yet reached the clinic.