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Updated: Jun 22, 2026

Bile Duct Ligation in Mice: Induction of Inflammatory Liver Injury and Fibrosis by Obstructive Cholestasis
Published on: February 10, 2015
[Pathogenesis of liver fibrosis in patients with chronic hepatitis B]
Jun Shi1, Jing-hua Hao, Wan-hua Ren
1Center for Liver Diseases, Provincial Hospital Affiliated to Shandong University, Jinan, China. sdshij@yahoo.com.cn
Insights
Sinusoidal endothelial cells interact with hepatic stellate cells, contributing to liver fibrosis. Early liver fibrosis involves microcirculation disorders and sinusoidal capillarization.
Area of Science:
- Hepatology
- Cell Biology
- Pathology
Context:
- Liver fibrosis is a significant health concern.
- Chronic hepatitis B can lead to liver fibrosis.
- The role of sinusoidal endothelial cells in fibrosis is not fully understood.
Purpose:
- To investigate the function of sinusoidal endothelial cells in liver fibrosis development.
- To clarify the relationship between hepatic microcirculation, sinusoidal capillarization, and liver fibrosis.
Summary:
- Liver biopsies from 56 chronic hepatitis B patients were analyzed using light and electron microscopy.
- Reduced fenestrations in sinusoidal endothelial cells and collagen deposition were observed.
- Hepatic stellate cell morphology resembled fibroblasts, with collagen fibers deposited around them.
Impact:
- Sinusoidal endothelial cells play a role in liver fibrosis through interaction with hepatic stellate cells.
- Hepatic microcirculation disorders and sinusoidal capillarization are early indicators of liver fibrosis.
- Findings provide insights into the cellular mechanisms underlying liver fibrosis progression.
Objective:
To explore the role of sinusoidal endothelial cell in the development of liver fibrosis, and to dissect the relationship among hepatic microcirculation disorders, hepatic sinusoidal capilarization and liver fibrosis.
Methods:
Liver biopsy was performed in fifty-six patients with chronic hepatitis B. The liver tissues were observed under light microscope and transmitted electronic microscope.
Results:
Of 56 cases, 39 cases were mild hepatitis, 10 were moderate hepatitis, and 7 were severe hepatitis. The morphology of hepatic stellate cells (HSCs) was similar to that of fibroblasts in the tissues of the patients with chronic hepatitis B. Collagenous fibers were deposited around the hepatic stellate cells. Electron-dense materials were deposited between sinusoidal endothelial cell and hepatic stellate cell. The size and amount of fenestraes of sinusoidal endothelial cells were reduced in 53 of 56 cases. The consecutive or inconsecutive membrane-like materials were observed along sinusoidal endothelial cells in 20 cases. Collagen fibers were observed in the space of Disse in 15 cases. Even in the patients with normal hepatic functions, red blood cells aggregation and microthrombi could be observed in the liver tissues.
Conclusion:
Sinusoidal endothelial cells are involved in development of liver fibrosis by interacting with hepatic stellate cells. Hepatic microcirculation disorders and sinusoidal capillarization are important changes in the early stage of liver fibrosis.
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