CoChat
Sign Up
Cited by 160Alcohol Consumption and Health EffectsLiver physiology and pathologyDrug-Induced Hepatotoxicity and Protection

Alcohol induced hepatic fibrosis: Role of acetaldehyde

Mello, Tommaso, Ceni, Elisabetta, Surrenti, Calogero, Galli, Andrea·2008·Molecular Aspects of Medicine
DOI 10.1016/j.mam.2007.10.001
Open this paper in CoChat — free account

Abstract

Alcohol abuse is one of the major causes of liver fibrosis worldwide. Although the pathogenesis of liver fibrosis is a very complex phenomenon involving different molecular and biological mechanisms, several lines of evidence established that the first ethanol metabolite, acetaldehyde, plays a key role in the onset and maintenance of the fibrogenetic process. This review briefly summarizes the molecular mechanisms underlying acetaldehyde pro-fibrogenic effects. Liver fibrosis represents a general wound-healing response to a variety of insults. Although mortality due to alcohol abuse has been constantly decreasing in the past 20 years in Southern Europe and North America, in several Eastern-European countries and Great Britain Alcoholic Liver Disease (ALD) shows a sharply increasing trend [Bosetti, C., Levi, F., Lucchini, F., Zatonski, W.A., Negri, E., La, V.C., 2007. Worldwide mortality from cirrhosis: an update to 2002. J. Hepatol. 46, 827-839]. ALD has a complex pathogenesis, in which acetaldehyde (AcCHO), the major ethanol metabolite, plays a central role. Ethanol is mainly metabolized in the liver by two oxidative pathways. In the first one ethanol is oxidized to acetaldehyde by the cytoplasmic alcohol dehydrogenase enzyme (ADH), acetaldehyde is then oxidized to acetic acid by the mitochondrial acetaldehyde dehydrogenase (ALDH). The second pathway is inducible and involves the microsomal ethanol-oxidizing system (MEOS), in which the oxidation of ethanol to acetaldehyde and acetic acid also leads to generation of reactive oxygen species (ROS). Chronic ethanol consumption significantly inhibits mitochondrial ALDH activity while the rate of ethanol oxidation to acetaldehyde is even enhanced, resulting in a striking increase of tissue and plasma acetaldehyde levels [Lieber, C.S., 1997. Ethanol metabolism, cirrhosis and alcoholism. Clin. Chim. Acta 257, 59-84]. This review will focus on the molecular mechanisms by which acetaldehyde promote liver fibrosis.

Integrity signals

Registry

Crossref · 10.1016/j.mam.2007.10.001

Cites

39 of 39 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • MAA adducts are found in HSCs, liver sinusoidal endothelial cells, and Kupffer cells in ALD models; they stimulate transformation of HSCs into activated myofibroblasts, resulting in elevated production of profibrotic factors such as PDGF, and can induce proinflammatory cytokines such as TNF-α, IL-12, IL-18, and MIF.

    “In addition to individual AA and MDA adducts, MAA adducts (AA-MDA-protein hybrid adducts) are found in HSCs, liver sinusoidal endothelial cells, and Kupffer cells in ALD models.”

    From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [220]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Related

Authors
Mello, T., Ceni, E., Surrenti, C., & Galli, A.
Affiliations
University of Florence (IT)
Corresponding author
Mello, Tommaso
ORCID
Venue
Molecular Aspects of Medicine
Publisher
Elsevier BV
Published
2008-02
Volume
29
Issue
1-2
Pages
17-21
ISSN
0098-2997 (ISSN-L)
DOI
10.1016/j.mam.2007.10.001
OpenAlex
W2063949300
Cited by
160
References
39
Citations by year
2026: 1 · 2025: 11 · 2024: 8 · 2023: 11 · 2022: 11 · 2021: 10 · 2020: 8 · 2019: 10 · 2018: 9 · 2017: 7 · 2016: 7 · 2015: 15 · 2014: 14 · 2013: 8 · 2012: 8
FWCI
0.56
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Molecular Aspects of Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • Florence Research (University of Florence) (submittedVersion)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
Keywords
acetaldehyde, alcoholic liver disease, alcohol metabolism, alcohol dehydrogenase, acetaldehyde dehydrogenase, microsomal ethanol oxidizing system, reactive oxygen species, fibrogenesis
MeSH terms
Acetaldehyde, Animals, Humans, Liver Cirrhosis, Liver Diseases, Alcoholic

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review