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

TL;DR

This review explores how multi-omics technologies help understand liver fibrosis and cirrhosis, offering new insights into their causes and potential treatments.

Contribution

The paper integrates human and animal model data using multi-omics to reveal shared mechanisms and therapeutic targets for liver fibrosis.

Findings

Multi-omics technologies reveal shared molecular pathways in liver fibrosis across different diseases.

Cross-species analysis validates animal models for human liver fibrosis research.

Systems-level insights from multi-omics aid in developing precision therapies and biomarkers.

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.

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