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Background <p>Liver fibrosis is a dynamic and reversible pathological process underlying chronic liver diseases, characterized by excessive extracellular matrix deposition and progressive hepatic architectural distortion. It acts as a critical precursor to cirrhosis, hepatic decompensation, and hepatocellular carcinoma, imposing a substantial global disease burden.</p> Main body <p>Accumulating evidence indicates that liver fibrosis is a highly plastic process governed by multicellular crosstalk, immune microenvironment remodeling, epigenetic–metabolic coupling, and mechanotransduction. This review outlines core cellular effectors and their heterogeneity revealed by single-cell omics, and highlights key regulatory layers including circadian rhythm, epigenetic imprinting, metabolic reprogramming, and the gut–liver axis, as well as etiology-specific differences in fibrosis progression, reversibility, and therapeutic response. We also summarize advances in non-invasive diagnosis and clinical translation of anti-fibrotic therapies, and discuss key bottlenecks leading to clinical trial failures. </p> Conclusion <p>A deeper understanding of cell fate regulation and multicellular ecosystem remodeling will facilitate the development of precise strategies to achieve meaningful fibrosis regression and improve long-term clinical outcomes in chronic liver diseases.</p>

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Mechanisms and reversal strategies of liver fibrosis: from regulation of cell fate to clinical translation

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月25日

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  • Chuhan Zeng,
  • Qiuxia Lu,
  • Qi Zhao,
  • Jian Li

摘要

Background

Liver fibrosis is a dynamic and reversible pathological process underlying chronic liver diseases, characterized by excessive extracellular matrix deposition and progressive hepatic architectural distortion. It acts as a critical precursor to cirrhosis, hepatic decompensation, and hepatocellular carcinoma, imposing a substantial global disease burden.

Main body

Accumulating evidence indicates that liver fibrosis is a highly plastic process governed by multicellular crosstalk, immune microenvironment remodeling, epigenetic–metabolic coupling, and mechanotransduction. This review outlines core cellular effectors and their heterogeneity revealed by single-cell omics, and highlights key regulatory layers including circadian rhythm, epigenetic imprinting, metabolic reprogramming, and the gut–liver axis, as well as etiology-specific differences in fibrosis progression, reversibility, and therapeutic response. We also summarize advances in non-invasive diagnosis and clinical translation of anti-fibrotic therapies, and discuss key bottlenecks leading to clinical trial failures.

Conclusion

A deeper understanding of cell fate regulation and multicellular ecosystem remodeling will facilitate the development of precise strategies to achieve meaningful fibrosis regression and improve long-term clinical outcomes in chronic liver diseases.