Liver fibrosis and cirrhosis in the multi-omics era: mechanisms and therapeutic perspectives from human and animal models.

Abstract

Liver fibrosis and cirrhosis are common outcomes of chronic liver diseases such as viral hepatitis, alcoholic liver disease, and non-alcoholic fatty liver disease. Despite diverse causes, they share core pathological features including hepatic stellate cell activation, extracellular matrix deposition, immune dysregulation, and metabolic alterations. Recent advances in multi-omics technologies-encompassing transcriptomics, proteomics, and metabolomics-enhance our understanding of the molecular and cellular mechanisms driving liver fibrosis. This review integrates findings from human studies and animal models, highlighting key pathological pathways and their interactions. Multi-omics analyses also clarify therapeutic mechanisms targeting oxidative stress, inflammation, and metabolic dysfunction. Cross-species comparisons confirm the translational relevance of animal models and underscore the value of multi-omics approaches in biomarker discovery and precision therapy development. Overall, these insights provide a systems-level understanding of liver fibrosis, facilitating advances in diagnosis and treatment strategies.