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 Experiment Videos

Liver fibrosis.

Ramón Bataller1, David A Brenner

  • 1Liver Unit, Institut de Malalties Digestives i Metabòliques, Hospital Clinic, Institut d'Investigació Biomèdiques August Pi i Sunyer (IDIBAPS),Barcelona, Catalonia, Spain.

The Journal of Clinical Investigation
|February 4, 2005
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

A translational model of MASLD-associated HFpEF defines mitochondrial dysfunction and cardiac plasticity during disease progression and regression.

Metabolism: clinical and experimental·2026
Same author

Precision pathophysiology in steatotic liver disease.

Clinical and molecular hepatology·2026
Same author

A Translational Model of MASLD-Associated HFpEF Defines Mitochondrial Dysfunction and Cardiac Plasticity During Disease Progression and Regression.

bioRxiv : the preprint server for biology·2026
Same author

Mesothelin/Mucin 16 Signaling in Activated Portal Fibroblasts Drives the Development of Cholestatic Fibrosis and Hepatocellular Carcinoma in Aged Female Multidrug Resistance Protein 2 Knockout Mice.

Cellular and molecular gastroenterology and hepatology·2026
Same author

Single-cell fixed RNA profiling uncovers SEMA4D and LMCD1 as therapeutic targets in a liver fibrosis model.

JHEP reports : innovation in hepatology·2026
Same author

RNA-binding protein LARP6 coordinates hepatic stellate cell activation and liver fibrosis.

The Journal of clinical investigation·2026
Same journal

Extracellular matrix reprogramming by the YAP/TAZ- TGF-ß2 axis drives immune exclusion in cholangiocarcinoma models.

The Journal of clinical investigation·2026
Same journal

Tumor cell-derived extracellular vesicles foster the immunosuppressive landscape of pancreatic cancer.

The Journal of clinical investigation·2026
Same journal

Julie Zikherman receives the ASCI/Marian W. Ropes, MD, Award.

The Journal of clinical investigation·2026
Same journal

Targeted degradation of MDM2 overcomes feedback regulation of p53 signaling in Merkel cell carcinoma models.

The Journal of clinical investigation·2026
Same journal

SGLT2 inhibitors enhance ketogenesis by acting as allosteric activators of the mitochondrial enzyme HMGCS2.

The Journal of clinical investigation·2026
Same journal

MDM2 degraders for Merkel cell carcinoma: round peg in a round hole.

The Journal of clinical investigation·2026
See all related articles

Liver fibrosis, a serious condition, involves excess collagen buildup. Recent findings show advanced liver fibrosis can be reversed, driving new drug development for treatment.

Area of Science:

  • Hepatology
  • Cellular Biology
  • Molecular Medicine

Background:

  • Liver fibrosis is characterized by excessive extracellular matrix deposition, primarily collagen, in chronic liver diseases.
  • Advanced stages lead to cirrhosis, liver failure, and portal hypertension, often necessitating liver transplantation.
  • Key collagen-producing cells include activated hepatic stellate cells, portal fibroblasts, and bone marrow-derived myofibroblasts.

Purpose of the Study:

  • To review recent advancements in understanding liver fibrosis pathogenesis and diagnosis.
  • To discuss emerging antifibrotic therapies targeting fibrogenic cells and extracellular matrix deposition.
  • To summarize current strategies for managing and potentially reversing liver fibrosis.

Main Methods:

  • Literature review of recent studies on liver fibrosis.

Related Experiment Videos

  • Analysis of cellular and molecular mechanisms driving fibrosis.
  • Evaluation of current and emerging antifibrotic therapeutic approaches.
  • Main Results:

    • Significant progress has been made in identifying cellular players and molecular signals (e.g., TGF-beta1, angiotensin II, leptin) in liver fibrosis.
    • The reversibility of advanced liver fibrosis in patients is a recent, significant finding.
    • Many experimental antifibrotic interventions show promise but require further human clinical validation.

    Conclusions:

    • Understanding liver fibrosis pathogenesis is crucial for developing effective treatments.
    • Emerging therapies focus on inhibiting fibrogenic cell activation and matrix deposition.
    • While promising, the clinical efficacy and safety of novel antifibrotic strategies require extensive investigation.