Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Cirrhosis II: Pathophysiology01:24

Cirrhosis II: Pathophysiology

Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to structural...
Liver Regeneration01:24

Liver Regeneration

The liver is an important organ in vertebrates that plays an essential role in metabolism. It is also responsible for storing and redistributing nutrients such as carbohydrates, fats, and vitamins in the body. Additionally, the liver releases bile salts which are critical for digesting food and eliminating toxic metabolites from the body.
Cells of Liver
The liver comprises four major types of cells— hepatocytes, stellate, Kupffer, and sinusoidal endothelial cells. The hepatocytes are large...
Cirrhosis I: Introduction01:23

Cirrhosis I: Introduction

Cirrhosis is a chronic, irreversible liver disease characterized by the widespread replacement of healthy liver tissue with fibrotic scar tissue and the formation of regenerative nodules.Etiology of cirrhosisCirrhosis results from sustained liver injury that triggers progressive fibrosis and structural remodeling. The underlying causes are diverse, encompassing common and less frequent clinical conditions. Regardless of the origin, all causes lead to chronic inflammation, hepatocyte loss, and...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Sigmoid Colon Metastasis from Endometrioid Carcinoma after a Long Disease-Free Interval Following Radiotherapy for Vaginal Recurrence: A Case Report and Review of the Literature.

Surgical case reports·2026
Same author

Good Responders to Rectal Cancer Neoadjuvant Chemotherapy, based on the MRI Findings Can Help to Avoid Radiotherapy: A Comparative Analysis.

Surgery today·2026
Same author

Clinical practice guidelines for telesurgery, 2nd Edition : Committee for the Promotion of Remote Surgery Implementation, Japan Surgical Society.

Surgery today·2026
Same author

Prognostic Power of Ensemble Learning in Colorectal Cancer with Peritoneal Metastasis: A Multi-Institutional Analysis.

Bioengineering (Basel, Switzerland)·2026
Same author

ASO Visual Abstract: Ki67 Gene Expression is Associated with Immune Cell Infiltration and Neoadjuvant Chemotherapy Response in ER+/HER2- Breast Cancer.

Annals of surgical oncology·2026
Same author

ASO Author Reflections: Does Ki67 Gene Expression Capture Immune Infiltration and Predict Chemotherapy Response in ER+/HER2- Breast Cancer?

Annals of surgical oncology·2026
Same journal

Phase II Trial of Nivolumab in Advanced Solid Tumors Based on Genomic Profiling: BELIEVE Trial (NCCH1901) Subcohort.

Cancer science·2026
Same journal

Urinary Small Extracellular Vesicle DNA as a Biomarker for the Non-Invasive Diagnosis of Bladder Cancer.

Cancer science·2026
Same journal

Splicing Factor Mutations in Clonal Hematopoiesis and Progression to Myeloid Neoplasms.

Cancer science·2026
Same journal

Genetic Evolution in BRCA1-Associated Breast Cancer Reveals Early Driver Mutations Shaping Tumor Features and Prognosis.

Cancer science·2026
Same journal

Hypericin Suppresses Liver Cancer Through Autophagic Degradation of AKT and Eliciting Antitumor Immune Response.

Cancer science·2026
Same journal

KYNU in Gastric Cancer Cells Promotes Tumor Progression by Influencing Macrophage Polarization Via PF4.

Cancer science·2026
See all related articles

Related Experiment Video

Updated: Jun 5, 2026

Seven Steps to Stellate Cells
06:40

Seven Steps to Stellate Cells

Published on: May 10, 2011

Decrease of hepatic stellate cells in rats with enhanced sensitivity to clofibrate-induced hepatocarcinogenesis.

Daisuke Yamana1, Takeshi Shimizu, Yang Fan

  • 1Department of Biochemistry and Genome Biology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.

Cancer Science
|January 11, 2011
PubMed
Summary
This summary is machine-generated.

Clofibrate treatment reduced hepatic stellate cells (HSC) in cancer-susceptible rats, correlating with preneoplastic lesion development. This loss was not directly caused by clofibrate toxicity.

More Related Videos

Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease with Fibrosis
06:26

Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease with Fibrosis

Published on: July 18, 2025

Related Experiment Videos

Last Updated: Jun 5, 2026

Seven Steps to Stellate Cells
06:40

Seven Steps to Stellate Cells

Published on: May 10, 2011

Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease with Fibrosis
06:26

Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease with Fibrosis

Published on: July 18, 2025

Area of Science:

  • Hepatology
  • Toxicology
  • Cell Biology

Background:

  • Nonparenchymal cells play a role in liver lesion development.
  • Clofibric acid (CF) is a known inducer of peroxisome proliferation and hepatomegaly.
  • Glutathione S-transferase M1 (GSTM1) gene polymorphisms influence cancer susceptibility.

Purpose of the Study:

  • To investigate the involvement of nonparenchymal cells in clofibrate-induced preneoplastic hepatic lesions.
  • To examine alterations in hepatic stellate cells (HSC) and Kupffer cells during lesion development.
  • To determine if clofibrate directly affects HSC viability or function.

Main Methods:

  • Immunohistochemical analysis of α-smooth muscle actin (α-SMA), vimentin, and CRBP1 in rat liver.
  • Administration of clofibrate (CF) to polymorphic rats (KS and NC types) for 4 and 8 weeks.
  • In vitro culture of human HSC with clofibric acid and gene expression analysis via microarray.

Main Results:

  • A significant decrease in α-SMA-positive HSC was observed in sensitive KS-type rats after 8 weeks of CF, but not in NC-type rats.
  • Kupffer cell numbers decreased similarly in both rat types; sinusoidal endothelial cells remained unchanged.
  • In vitro studies indicated that clofibrate did not directly induce HSC loss or alter HSC marker gene expression.

Conclusions:

  • The loss of HSC in cancer-susceptible rats treated with clofibrate may be linked to the development of preneoplastic hepatic lesions.
  • This HSC depletion is likely an indirect effect of clofibrate, not a direct toxic insult.
  • Further research is needed to elucidate the precise mechanisms connecting HSC loss and preneoplastic foci formation.