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

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...
Ultrasound II: Endoscopic Ultrasound and FibroScan01:25

Ultrasound II: Endoscopic Ultrasound and FibroScan

Endoscopic Ultrasound (EUS) and FibroScan are valuable diagnostic tools in gastroenterology and hepatology, each with specific applications and techniques.
Endoscopic Ultrasound (EUS):
Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow01:26

Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow

Chronic liver disease significantly impacts drug metabolism due to alterations in hepatic blood flow and enzyme accessibility. This disruption affects the body's pharmacokinetics—the movement and processing of drugs within the system. Key enzymes crucial for metabolizing medications become less accessible, changing how drugs are processed and utilized. Furthermore, liver disease influences the synthesis of plasma proteins, such as albumin and globulins, which play critical roles in drug binding...
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...
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...

You might also read

Related Articles

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

Sort by
Same author

Gastric mucosal brushing enhances gastric microbiome profiling compared with conventional biopsy in gastric cancer.

Scientific reports·2026
Same author

Validation of Risk Models for Predicting Post-SVR HCC in Real-World Surveillance Across Global Geographic Regions.

Liver international : official journal of the International Association for the Study of the Liver·2026
Same author

The small interfering RNA imdusiran as single and multiple doses in healthy, randomised individuals and non-randomised individuals with chronic hepatitis B (AB-729-001): a phase 1a/b trial.

The lancet. Gastroenterology & hepatology·2026
Same author

Angptl4 integrates dietary and microbial signals to disrupt gut barrier function in MASH.

Nature communications·2026
Same author

Development of a longitudinal predictive model for hepatocellular carcinoma occurrence in patients with chronic hepatitis B.

Scientific reports·2026
Same author

Host Factors DDB2 and DNA Polymerase Delta Are Linked to cccDNA Persistence in Hepatitis B Virus and Occult Hepatitis B Virus-Related Hepatocellular Carcinoma.

Journal of viral hepatitis·2026

Related Experiment Video

Updated: Jun 25, 2026

Bile Duct Ligation in Mice: Induction of Inflammatory Liver Injury and Fibrosis by Obstructive Cholestasis
08:56

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

Published on: February 10, 2015

Cirrhosis--can we reverse hepatic fibrosis?

Pisit Tangkijvanich1, Hal F Yee

  • 1Department of Medicine (Digestive Diseases), UCLA School of Medicine, Los Angeles, California 90095, USA.

The European Journal of Surgery. Supplement. : = Acta Chirurgica. Supplement
|September 8, 2005
PubMed
Summary

Cirrhosis results from liver fibrosis, primarily driven by activated hepatic stellate cells. Targeting these cells and their signaling pathways, like TGF-beta, shows promise for slowing or reversing liver fibrosis.

Area of Science:

  • Hepatology
  • Cellular Biology
  • Pathophysiology

Background:

  • Cirrhosis, characterized by liver fibrosis, is a major cause of morbidity and mortality from chronic liver diseases.
  • Current treatments target specific causes of liver injury but lack efficacy for many conditions.
  • Advances in understanding liver fibrosis mechanisms have identified hepatic stellate cells as key players.

Purpose of the Study:

  • To review the understanding of hepatic fibrosis and cirrhosis mechanisms.
  • To highlight the role of hepatic stellate cells in liver fibrosis.
  • To explore novel therapeutic targets for liver fibrosis based on molecular and cellular mechanisms.

Main Methods:

  • Review of recent investigations into the pathophysiology of liver fibrosis.

More Related Videos

Development of an Ethanol-induced Fibrotic Liver Model in Zebrafish to Study Progenitor Cell-mediated Hepatocyte Regeneration
10:42

Development of an Ethanol-induced Fibrotic Liver Model in Zebrafish to Study Progenitor Cell-mediated Hepatocyte Regeneration

Published on: May 13, 2016

Isolation of Regenerating Hepatocytes after Partial Hepatectomy in Mice
10:04

Isolation of Regenerating Hepatocytes after Partial Hepatectomy in Mice

Published on: December 2, 2022

Related Experiment Videos

Last Updated: Jun 25, 2026

Bile Duct Ligation in Mice: Induction of Inflammatory Liver Injury and Fibrosis by Obstructive Cholestasis
08:56

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

Published on: February 10, 2015

Development of an Ethanol-induced Fibrotic Liver Model in Zebrafish to Study Progenitor Cell-mediated Hepatocyte Regeneration
10:42

Development of an Ethanol-induced Fibrotic Liver Model in Zebrafish to Study Progenitor Cell-mediated Hepatocyte Regeneration

Published on: May 13, 2016

Isolation of Regenerating Hepatocytes after Partial Hepatectomy in Mice
10:04

Isolation of Regenerating Hepatocytes after Partial Hepatectomy in Mice

Published on: December 2, 2022

  • Analysis of signal transduction pathways linking hepatic injury to stellate cell function.
  • Examination of studies on therapeutic interventions, including TGF-beta receptor antagonism.
  • Main Results:

    • Hepatic stellate cells are central to hepatic fibrosis development and cirrhosis progression.
    • Stellate cell activation involves chemotaxis, proliferation, contraction, fibrogenesis, and matrix degradation.
    • Modulating stellate cell signaling, such as TGF-beta antagonism, shows potential in animal models to slow or reverse fibrosis.

    Conclusions:

    • A deeper understanding of the molecular and cellular basis of cirrhosis offers new therapeutic avenues.
    • Targeting hepatic stellate cell activation and signaling pathways presents a rational approach to treating liver fibrosis.
    • These findings may significantly impact the clinical management of patients with chronic liver disease.