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Updated: Jul 7, 2026

Mapping Hepatic Stellate Cell Morphology in Mouse Models of Liver Fibrosis
Published on: February 13, 2026
[Correlation between liver stem cell activation and histopathologic changes in liver with hepatic failure]
Ying-yan Yu1, Jun Ji, Shan Jiang
1Division of Pathology, Organ Transplantation Center and Shanghai Institute of Digestive Surgery of Ruijin Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200025, China. yingyan3y@yahoo.com.cn
Objective:
To investigate the correlation between liver stem cell activation and histopathologic changes in liver transplant recipients with hepatic failure.
Methods:
A total of 33 cases of hepatic failure were enrolled into the study. Donor liver tissues were used as normal controls. Histopathologic changes, presence of hepatotropic virus antigens, history of artificial liver therapy and number of c-kit positive cells were analyzed.
Results:
There were a total of 25 males and 8 females. The age of patients ranged from 21 to 64 years. Among the 33 patients studied, 6 suffered from acute liver failure, 5 from subacute liver failure and the remaining from acute-on-chronic liver failure (associated with cirrhosis). Thirteen patients had a history of artificial liver therapy. Activated liver stem cells expressed c-kit monoclonal antibody but were negative for toluidine blue stain. The number of c-kit-positive cells in acute liver failure, subacute liver failure and acute-on-chronic liver failure were 3.50 +/- 2.66 (0 to 8) per mm(2), 11.47 +/- 8.85 (3 to 30) per mm(2) and 15.50 +/- 10.95 (5 to 45) per mm(2), respectively (P < 0.05). The number of c-kit-positive cells in cases with or without artificial liver therapy showed no statistically significant difference.
Conclusions:
The poor prognosis of acute liver failure is mainly due to massive liver necrosis and insufficient stem cell activation. Liver stem cell level is increased whenever there is progression into subacute liver failure and chronic liver failure. Actively treating acute liver failure with stimulation of the self-regeneration system in liver is thus useful.
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