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Updated: May 15, 2026

Isolation of Rat Portal Fibroblasts by In situ Liver Perfusion
Published on: June 29, 2012
Origin of myofibroblasts in liver fibrosis
David A Brenner1, Tatiana Kisseleva1, David Scholten1
1University of California, San Diego, School of Medicine, San Diego, CA, USA.
Abstract:
Most chronic liver diseases of all etiologies result in progressive liver fibrosis. Myofibroblasts produce the extracellular matrix, including type I collagen, which constitutes the fibrous scar in liver fibrosis. Normal liver has little type I collagen and no detectable myofibroblasts, but myofibroblasts appear early in experimental and clinical liver injury. The origin of the myofibroblast in liver fibrosis is still unresolved. The possibilities include activation of endogenous mesenchymal cells including fibroblasts and hepatic stellate cells, recruitment from the bone marrow, and transformation of epithelial or endothelial cells to myofibroblasts. In fact, the origin of myofibroblasts may be different for different types of chronic liver diseases, such as cholestatic liver disease or hepatotoxic liver disease. This review will examine our current understanding of the liver myofibroblast.
Insights
Liver fibrosis, a hallmark of chronic liver disease, involves myofibroblasts producing scar tissue. Their precise origin in liver fibrosis remains an active area of research and investigation.
Area of Science:
- Hepatology
- Cell Biology
- Fibrosis Research
Background:
- Chronic liver diseases lead to progressive liver fibrosis.
- Myofibroblasts are key cells in producing the fibrous scar tissue (extracellular matrix, including type I collagen) characteristic of liver fibrosis.
- Myofibroblasts are present early in liver injury, but their origin in fibrosis is not fully understood.
Purpose of the Study:
- To review the current understanding of the origin of myofibroblasts in liver fibrosis.
- To explore potential sources of myofibroblasts, including endogenous mesenchymal cells, bone marrow recruitment, and cell transformation.
- To consider if myofibroblast origins differ among various chronic liver disease etiologies.
Main Methods:
- Literature review of experimental and clinical studies on liver fibrosis.
- Analysis of research investigating myofibroblast origins in different liver disease models.
- Synthesis of current knowledge on hepatic stellate cell activation, bone marrow-derived cell contribution, and epithelial-to-myofibroblast transition.
Main Results:
- Myofibroblasts are central to scar formation in liver fibrosis.
- Several potential origins for myofibroblasts exist, including hepatic stellate cells and potentially other cell types.
- The specific origin of myofibroblasts may vary depending on the underlying cause of liver disease.
Conclusions:
- The origin of myofibroblasts in liver fibrosis is complex and likely multifactorial.
- Understanding myofibroblast origins is crucial for developing targeted therapies for liver fibrosis.
- Further research is needed to elucidate the distinct pathways contributing to myofibroblast populations in diverse chronic liver diseases.
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