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Related Experiment Video

Updated: Mar 20, 2026

Bile Duct Ligation in Mice: Induction of Inflammatory Liver Injury and Fibrosis by Obstructive Cholestasis

Bile Duct Ligation in Mice: Induction of Inflammatory Liver Injury and Fibrosis by Obstructive Cholestasis

Published on: February 10, 2015

Treating Liver Fibrosis: (Re)Programmed to Succeed.

Yuan Guan¹, Dan Xu¹, Gary Peltz¹

¹Department of Anesthesia, Stanford University School of Medicine, Stanford, CA 94305, USA.

|June 4, 2016

Summary

Scientists reprogrammed mouse liver cells into hepatocyte-like cells using transcription factors. This innovative approach shows promise for treating liver cirrhosis in preclinical models.

Area of Science:

Stem cell biology
Hepatology
Regenerative medicine

Background:

Liver fibrosis and cirrhosis are significant health concerns.
Current treatments for liver disease have limitations.
Myofibroblasts are key cells implicated in liver scarring.

Purpose of the Study:

To investigate the potential of direct cellular reprogramming for liver regeneration.
To convert liver myofibroblasts into functional hepatocyte-like cells.
To evaluate the therapeutic efficacy of this reprogramming strategy in murine liver injury models.

Main Methods:

Utilized transcription factor-mediated direct reprogramming.
Targeted liver myofibroblasts for conversion into hepatocyte-like cells.
Employed mouse models of fibrotic and cholestatic liver injury.

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Last Updated: Mar 20, 2026

Bile Duct Ligation in Mice: Induction of Inflammatory Liver Injury and Fibrosis by Obstructive Cholestasis

Bile Duct Ligation in Mice: Induction of Inflammatory Liver Injury and Fibrosis by Obstructive Cholestasis

Published on: February 10, 2015

Murine Precision-Cut Liver Slices as an Ex Vivo Model of Liver Biology

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Published on: March 14, 2020

Three-Dimensional Collagen Matrix Scaffold Implantation as a Liver Regeneration Strategy

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Published on: June 29, 2021

Main Results:

Successfully reprogrammed liver myofibroblasts into hepatocyte-like cells in mice.
Demonstrated the potential of this method in models of liver injury.
Provided proof-of-concept for a novel regenerative approach.

Conclusions:

Transcription-factor-mediated reprogramming offers a promising avenue for liver regeneration.
This strategy holds potential for developing new therapies for liver cirrhosis.
Further research is warranted to translate this finding into clinical applications.