Alcoholic Liver Disease: Pathogenesis and New Therapeutic Targets

Gao, Bin; Bataller, Ramon

doi:10.1053/j.gastro.2011.09.002

Cited by 1,963Alcohol Consumption and Health EffectsLiver physiology and pathologyLiver Disease and Transplantation

Alcoholic Liver Disease: Pathogenesis and New Therapeutic Targets

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Gao, Bin, Bataller, Ramon·2011·Gastroenterology

DOI 10.1053/j.gastro.2011.09.002PMC PMC3214974

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Abstract

Alcoholic liver disease (ALD) is a major cause of chronic liver disease worldwide and can lead to fibrosis and cirrhosis. The latest surveillance report published by the National Institute on Alcohol Abuse and Alcoholism showed that liver cirrhosis was the 12th leading cause of death in the United States, with a total of 29,925 deaths in 2007, 48% of which were alcohol related. The spectrum of ALD includes simple steatosis, alcoholic hepatitis, fibrosis, cirrhosis, and superimposed hepatocellular carcinoma. Early work on the pathogenesis of the disease focused on ethanol metabolism-associated oxidative stress and glutathione depletion, abnormal methionine metabolism, malnutrition, and production of endotoxins that activate Kupffer cells. We review findings from recent studies that have characterized specific intracellular signaling pathways, transcriptional factors, aspects of innate immunity, chemokines, epigenetic features, microRNAs, and stem cells that are associated with ALD, improving our understanding of its pathogenesis. Despite this progress, no targeted therapies are available. The cornerstone of treatment for alcoholic hepatitis remains as it was 40 years ago: abstinence, nutritional support, and corticosteroids. There is an urgent need to develop new pathophysiology-oriented therapies. Recent translational studies of human samples and animal models have identified promising therapeutic targets.

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Alcoholic fatty liver is observed in up to 90% of heavy drinkers.
“Alcoholic fatty liver is defined by fat accumulation in hepatocytes without substantial inflammation, or hepatic fibrosis, and is observed in up to 90% of heavy drinkers [9,11,12,13,14].”
From Pathophysiological Aspects of Alcohol Metabolism in the Liver (2021) · cites this paper as [11]
The Spectrum, Risk Factors, and Comorbidities section says fatty liver develops in more than 90% of heavy drinkers. That contradicts the attributed figure of up to 90%. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measured
Alcoholic liver disease (ALD) is caused by chronic or binge consumption of alcohol.
“Alcoholic liver disease (ALD) is a globally prevalent chronic liver disease caused by chronic or binge consumption of alcohol.”
From Pathophysiological Aspects of Alcohol Metabolism in the Liver (2021) · cites this paper as [11]
The Abstract describes alcohol as a major cause of chronic liver disease, and “Spectrum, Risk Factors, and Comorbidities” links heavy drinking to ALD. That section also compares daily heavy drinking with episodic or binge drinking, but it does not establish that binge drinking alone causes ALD. (LLM, conf=0.82)
Experimental — accuracy not yet measured
Heavy long-term alcohol consumption accelerates the transition of alcoholic fatty liver into alcoholic hepatitis.
“Heavy long-term alcohol consumption accelerates the transition of alcoholic fatty liver into alcoholic hepatitis, which is characterized by steatosis, ballooning hepatocytes, and infiltration of neutrophils with or without fibrosis [11,12,13,14,15,16].”
From Pathophysiological Aspects of Alcohol Metabolism in the Liver (2021) · cites this paper as [11]
The Spectrum, Risk Factors, and Comorbidities section says fatty liver is an early response to heavy drinking and that alcoholic hepatitis may occur in patients with underlying alcoholic liver disease and heavy alcohol intake. The Pathogenesis > AH section says hepatitis develops in patients with steatosis and describes ballooning hepatocytes, neutrophilic infiltration, steatosis, and fibrosis. These passages support the progression and histologic description, but do not establish that long-term heavy drinking accelerates the specific transition from fatty liver to hepatitis. (LLM, conf=0.85)
Experimental — accuracy not yet measured
Alcohol metabolism generates products that damage the liver, resulting in ALD.
“Alcohol metabolism generates products that damage the liver, resulting in alcoholic liver disease (ALD), a main cause of chronic liver disease [4,9,10,11].”
From Pathophysiological Aspects of Alcohol Metabolism in the Liver (2021) · cites this paper as [11]
HBV promotes steatosis through inducing mitochondrial dysfunction and peroxisome proliferator-activated receptors by the HBx protein.
“through inducing mitochondrial dysfunction and peroxisome proliferator-activated receptors by the HBx protein [94]”
From Etiology-Based Treatment for Unresectable/Advanced Hepatocellular Carcinoma: Focus on Viral Hepatitis and Metabolic Dysfunction-Associated Steatohepatitis (2025) · cites this paper as [94]
The “Alcoholic Fatty Liver (Steatosis)” section links disrupted mitochondrial fatty-acid oxidation and PPAR-α inactivation to alcohol-induced steatosis, not to HBV or HBx. The “Spectrum, Risk Factors, and Comorbidities” section mentions hepatitis B only in connection with alcohol’s effects on liver-disease progression. Searches for HBx and HBV-induced steatosis found no passage addressing the claimed mechanism; page numbers were not available in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measured

Alcohol use can also cause an inflammatory response known as alcoholic hepatitis, or steatohepatitis if it is accompanied by hepatic lipid deposition.
“Alcohol use can also cause an inflammatory response known as alcoholic hepatitis, or steatohepatitis if it is accompanied by hepatic lipid deposition.”
From The relationship between different dimensions of alcohol use and the burden of disease—an update (2017) · cites this paper as [279]
Alcohol use, especially heavy drinking occasions, induces changes in lipid metabolism resulting in the accumulation of lipids in hepatocytes called fatty liver.
“Alcohol use, especially heavy drinking occasions, induces changes in lipid metabolism (increases lipogenesis and mobilization of lipids and simultaneously decreases hepatic lipid catabolism), resulting in the accumulation of lipids in hepatocytes called fatty liver.”
From The relationship between different dimensions of alcohol use and the burden of disease—an update (2017) · cites this paper as [279]
Although hepatic steatosis does not normally cause irreversible hepatic changes, persistence and severity of alcoholic hepatitis or steatohepatitis leads eventually to fibrosis and sclerotic changes in the liver that result in liver cirrhosis and subsequent liver failure.
“Although hepatic steatosis does not normally cause irreversible hepatic changes, persistence and severity of alcoholic hepatitis or steatohepatitis leads eventually to fibrosis and sclerotic changes in the liver that result in insidious replacement of hepatocytes with connective tissue (liver cirrhosis) and subsequent liver failure.”
From The relationship between different dimensions of alcohol use and the burden of disease—an update (2017) · cites this paper as [279]
Alcoholic liver disease accounts for about half of all cirrhosis cases and is a cofactor in liver disease caused by HBV, HCV and NASH.
“ALD contributes to about half of all cirrhosis cases41 and is a cofactor in liver disease induced by HBV, HCV and NASH.”
From The gut microbiome and liver cancer: mechanisms and clinical translation (2017) · cites this paper as [41]
Chronic and excessive alcohol intake is known to cause liver injury from mild steatosis (AFLD) to more advanced liver disease such as ASH, fibrosis/cirrhosis, hepatic cancer, liver failure, and death.
“Chronic and excessive alcohol intake is known to cause liver injury from mild steatosis (simple fat accumulation in so-called alcoholic fatty liver disease, AFLD) to more advanced liver disease such as inflammation (alcoholic steatohepatitis, ASH), fibrosis/cirrhosis, hepatic cancer, liver failure, and death203–213.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [208]
Continued mitochondrial dysfunction with increased oxidative stress sensitizes hepatocytes to subsequent necrosis and/or apoptosis, which likely leads to activation of Kupffer cells and recruitment of infiltrating immune cells with elevated hepatic inflammation and pro-inflammatory cytokines/chemokines.
“Continued mitochondrial dysfunction with increased oxidative stress also sensitizes the hepatocytes to subsequent necrosis and/or apoptosis of hepatocytes, which likely lead to activation of resident liver macrophage (i.e., Kupffer cells) and recruitment of infiltrating immune cells into the liver with elevated levels of hepatic inflammation (steatohepatitis) and pro-inflammatory cytokines/chemok”
From Mitochondrial dysfunction and tissue injury by alcohol, high fat, nonalcoholic substances and pathological conditions through post-translational protein modifications (2014) · cites this paper as [14]

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“Aside from co-existent MAFLD and viral hepatitis, the effects of alcohol on steatosis, accelerated cirrhosis, and hepatocarcinogenesis in patients with viral hepatitis are well established [95, 96].”

Authors: Gao, B., & Bataller, R.
Affiliations: National Institutes of Health (US)
Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (ES)
Corresponding author: Gao, Bin
Bataller, Ramon
ORCID: Gao, Bin
Bataller, Ramon
Venue: Gastroenterology
Publisher: Elsevier BV
Published: 2011-11
Volume: 141
Issue: 5
Pages: 1572-1585
ISSN: 0016-5085 (ISSN-L)
DOI: 10.1053/j.gastro.2011.09.002
PMC: PMC3214974
OpenAlex: W2060637877
Cited by: 1,963
References: 161
Citations by year: 2026: 104 · 2025: 125 · 2024: 132 · 2023: 134 · 2022: 149 · 2021: 162 · 2020: 164 · 2019: 151 · 2018: 154 · 2017: 143 · 2016: 135 · 2015: 142 · 2014: 120 · 2013: 84 · 2012: 56
FWCI: 10.54
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Gastroenterology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health (Z99‐AA999999)
National Institute on Alcohol Abuse and Alcoholism (ZIAAA000369)
Topics: Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Health Sciences › Medicine › Hepatology › Liver Disease and Transplantation
Keywords: alcoholic liver disease, alcoholic hepatitis, liver fibrosis, liver cirrhosis, alcohol metabolism, oxidative stress, glutathione depletion, methionine metabolism, Kupffer cells, endotoxin, intracellular signaling, transcription factors, innate immunity, chemokines, epigenetics, microRNA, stem cells, therapeutic target, corticosteroids, nutritional support
MeSH terms: Adrenal Cortex Hormones, Alcohol Drinking, Humans, Liver Diseases, Alcoholic, Temperance, Liver Transplantation, Oxidative Stress, Nutritional Support

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Alcoholic Liver Disease: Pathogenesis and New Therapeutic Targets

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