Alcohol-Induced Liver Disease: Clinical, Molecular Mechanism, Pathology, Therapeutics

A Special Issue of Livers (ISSN 2673-4389).

Deadline for manuscript submissions: 20 January 2027 | Viewed by 865

Editors


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Guest Editor
In Vitro Drug Safety and Biotechnology and Department of Pharmacology and Toxicology, Faculty of Medicine, Banting Institute, University of Toronto, 100 College Street, Toronto, ON M5G 1L5, Canada
Interests: alcoholic liver disease; non-alcoholic steatohepatitis; hepatocytotoxicity; inflammatory biomarkers
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Special Issue Information

Dear Colleagues,

Alcohol-induced Liver Disease (ALD) is presented as steatosis caused by alcohol misuse. Often, ALD occurs in conjunction with other metabolic disorders such as high cholesterol, obesity, and diabetes. ALD is underdiagnosed due to a lack of evidence of heavy drinking or symptoms. Alcoholic Steatohepatitis (ASH) is a severe form of ALD, where fibrosis of the liver tissue occurs. It is a serious condition that can progress to cirrhosis and potentially result in the need for liver transplantation or death. 

Other possible subjects include the following:

  1. Consumption of alcoholic beverages belongs to the everyday "diet" in many countries, independent of the time of the day, during meals or outside of the meals, and independent of the type of alcohol. This has to be taken into account when approaching a patient with ALD. Often, in fact, it may be difficult to diagnose a pure alcoholic liver disease, to establish a follow-up schedule to eventually prevent liver cirrhosis and cancer development.
  2. History of liver cirrhosis and HCC development before and after the era of viral hepatitis in the Western world.
  3. Alcoholic beverage and tobacco consumption: synergistic damaging noxae?
  4. ALD and distilled alcoholic beverages.
  5. Diagnostic tests of alcohol consumption.
  6. Animal models of alcoholic liver damage.
  7. Sugar (glucose, fructose, xylose) and alcohol consumption synergistic effects in liver damage.

Prof. Dr. Giuliano Ramadori
Prof. Dr. Manuela G. Neuman
Guest Editors

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Keywords

  • alcohol-induced liver damage
  • acute alcoholic hepatitis
  • viruses and alcohol drinking
  • models of alcohol toxicity
  • hyper-glycemia and alcohol
  • fructose, glucose and alcohol liver disease
  • role of alcohol industry in safe drinking

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Published Papers (1 paper)

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Review

25 pages, 6768 KB  
Review
Fructose and Alcohol Hepatotoxicity: Demographic Overlap and Mechanistic Interactions
by Arthur D. Stem, Athina Lisgara, Mohammad Alayyoub, Domenica Berardi, Oladimeji Aladelokun, Caroline H. Johnson, Richard J. Johnson and Vasilis Vasiliou
Livers 2026, 6(5), 92; https://doi.org/10.3390/livers6050092 - 4 Sep 2026
Viewed by 301
Abstract
As metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-associated liver disease (ALD) grow increasingly prevalent, it is essential to improve understanding of the contributing factors and how these conditions may interact. Metabolic and alcohol-related liver injury frequently co-occur, prompting the introduction of the [...] Read more.
As metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-associated liver disease (ALD) grow increasingly prevalent, it is essential to improve understanding of the contributing factors and how these conditions may interact. Metabolic and alcohol-related liver injury frequently co-occur, prompting the introduction of the term metabolic dysfunction and alcohol-associated liver disease (MetALD) to describe individuals with MASLD who also consume significant amounts of alcohol. Among the exposures relevant to MetALD, dietary fructose is of particular interest because it shares multiple mechanisms of hepatotoxicity with alcohol. This review synthesizes current evidence for hepatotoxic interactions, emphasizing areas most relevant to MetALD pathogenesis. Epidemiologic data indicate substantial overlap between populations with high fructose and alcohol exposure, while clinical studies increasingly associate combined exposure with greater fibrosis progression and adverse liver outcomes. Several mechanistic pathways have been shown to overlap in terms of their interactions with fructose and ethanol, including endogenous fructose generation, cytochrome P450 2E1 (CYP2E1) induction, mitochondrial dysfunction, dysregulated lipid metabolism, uric acid-driven inflammasome signaling, and disruption of the gut–liver axis. Emerging evidence suggests that these pathways interact in ways that may amplify injury beyond the effects of either exposure alone. Greater integration of the alcohol and metabolic liver disease fields will be necessary to clarify mechanistic interactions, determine risk factors, and develop effective interventions for this increasingly common form of liver injury. Full article
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