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Related Experiment Video

Updated: Jun 23, 2026

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen

Published on: November 27, 2019

Signalling pathways in alcohol-induced liver inflammation.

Pranoti Mandrekar¹, Gyongyi Szabo

¹Department of Medicine, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA. pranoti.mandrekar@umassmed.edu

Journal of Hepatology

|April 29, 2009

Summary

Alcoholic liver disease involves complex cell signaling. Alcohol sensitizes liver macrophages to endotoxin, triggering inflammatory pathways like Toll-like receptor 4 (TLR4) and MAPK, driving liver injury.

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Histological Analyses of Acute Alcoholic Liver Injury in Zebrafish

Histological Analyses of Acute Alcoholic Liver Injury in Zebrafish

Published on: May 25, 2017

Area of Science:

Hepatology
Immunology
Molecular Biology

Background:

Alcoholic liver disease (ALD) pathogenesis involves intricate intracellular signaling pathways within liver cells.
A key feature of ALD is alcohol-induced sensitization of liver macrophages to endotoxin/lipopolysaccharide (LPS).

Purpose of the Study:

To review the critical intracellular signaling mechanisms underlying alcohol-induced inflammation in ALD.
To highlight the role of LPS-induced signaling pathways in the initiation and progression of alcoholic liver injury.

Main Methods:

This review synthesizes current research on molecular signaling pathways in ALD.
Focuses on Toll-like receptor 4 (TLR4) and mitogen-activated protein kinase (MAPK) pathways.
Examines the interplay between alcohol, reactive oxygen species, and inflammatory responses.

Main Results:

LPS recognition by TLR4 activates downstream pathways, including NF-kappaB and AP-1 transcription factors.
Activation of MAPK pathways (ERK, p38) contributes significantly to liver injury.
Alcohol-induced reactive oxygen species interact with TLR pathways, exacerbating inflammation.

Conclusions:

Key signaling intermediates drive alcohol-induced inflammation in alcoholic liver disease.
Understanding these pathways is crucial for developing therapeutic strategies for ALD.
The interplay between TLRs, MAPK, and oxidative stress is central to ALD pathogenesis.