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Related Concept Videos

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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...
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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
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Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
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Regulation of Angiogenesis and Blood Supply

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Related Experiment Video

Updated: Jun 5, 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

Cholangiocyte RUNX1 Orchestrates Fibrogenic and Inflammatory Signaling to Drive Biliary Fibrosis.

Sayed Obaidullah Aseem, Jing Wang, Ahmed Younis

    Biorxiv : the Preprint Server for Biology
    |June 4, 2026
    PubMed
    Summary

    Runt-related transcription factor 1 (RUNX1) drives biliary fibrosis and inflammation in cholangiopathies. Inhibiting RUNX1 reduces these processes, suggesting it as a therapeutic target for primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC).

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    Last Updated: Jun 5, 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

    A Mouse Model of Chronic Liver Fibrosis for the Study of Biliary Atresia
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    Published on: February 3, 2023

    Murine Precision-Cut Liver Slices as an Ex Vivo Model of Liver Biology
    12:36

    Murine Precision-Cut Liver Slices as an Ex Vivo Model of Liver Biology

    Published on: March 14, 2020

    Area of Science:

    • Hepatology and immunology
    • Molecular biology and genetics
    • Cholangiocyte biology

    Background:

    • Biliary fibrosis and inflammation are key in cholangiopathies like PSC and PBC.
    • Transcriptional mechanisms in cholangiocytes driving these processes are not fully understood.
    • Transforming growth factor-β (TGFβ) and lipopolysaccharide (LPS) are known fibrogenic and inflammatory stimuli.

    Purpose of the Study:

    • To investigate the role of Runt-related transcription factor 1 (RUNX1) as a transcriptional co-regulator in cholangiocyte fibroinflammatory signaling.
    • To determine if RUNX1 inhibition can attenuate biliary fibrosis and inflammation.

    Main Methods:

    • RUNX1 knockdown and pharmacologic inhibition in human PSC-derived cholangiocytes (PSC-Cs) and mouse biliary epithelial cells (MLEs).
    • Cytokine profiling, ChIP-qPCR, ChIP-seq, and LC-MS/MS to assess RUNX1 binding and interactions.
    • In vivo studies using Mdr2-/- mice and cholangiocyte-specific Runx1 knockout mice challenged with DDC diet.

    Main Results:

    • RUNX1 expression was elevated in cholangiocytes from PSC/PBC patients and Mdr2-/- mice.
    • RUNX1 inhibition reduced pro-inflammatory cytokines (IL6, TNFα) and attenuated TGFβ/LPS-induced gene expression.
    • RUNX1 binds to the IL6 promoter and other inflammatory gene sites, interacting with SMAD2 and NFκB2.
    • In vivo, RUNX1 inhibition reduced fibrosis, inflammation, and liver injury markers.

    Conclusions:

    • RUNX1 acts as a central transcriptional hub integrating TGFβ and inflammatory signals in cholangiocytes.
    • RUNX1 inhibition effectively reduces biliary fibrosis and inflammation in cholestatic models.
    • RUNX1 represents a promising therapeutic target for fibroinflammatory cholangiopathies.