Regression of liver cirrhosis

Cirrhosis prevalence and mortality continue to rise globally, with a >50% increase in cases since 1990, imposing a growing burden through chronic healthcare needs, recurrent hospitalisation, and liver transplantation, which remains the only definitive cure for advanced disease. Long regarded as a fixed end-stage, cirrhosis is now recognised as a dynamic and modifiable disease state. Sustained aetiological control can induce meaningful architectural remodelling, and single-cell and spatial analyses show that cirrhosis is a heterogeneous fibrotic niche shaped by context-specific fibrogenic, immune, and vascular cell phenotypes. Thus, reversibility is determined not simply by fibrosis stage, but by the biological state of the scar and its microenvironment. Nevertheless, recent disappointing antifibrotic trials, particularly in MASH-related cirrhosis, highlight the structural resilience of advanced disease and the limited sensitivity of conventional histological endpoints. Moreover, although structural improvement appears to confer measurable prognostic benefit, regression does not equate to complete restoration of tissue homeostasis, and residual vascular dysfunction and oncogenic risk often persist. Translating emerging mechanistic insights into precise measurement tools and effective therapies for cirrhosis regression now represents a central challenge in hepatology.