Evidence map›Paper›PMID 18242193›Full record

ReviewFree radical biology & medicine2008

Mitochondrial dysfunction and oxidative stress in the pathogenesis of alcohol- and obesity-induced fatty liver diseases.

Sudheer K Mantena, Adrienne L King, Kelly K Andringa, Heather B Eccleston, Shannon M Bailey

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 194 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
194citing papers in PubMed, 2 pooled it
18.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

194 citing papers in PubMed, 2 syntheses or guidelines pooled it, 417 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Article
  6. Food science & nutrition · 2026
    Article
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  10. Review
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  15. Therapeutic Power of Date Fruit (Food science & nutrition · 2025
    Review
  16. Article
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  18. New Application of an Old Drug: Anti-Diabetic Properties of Phloroglucinol.International journal of molecular sciences · 2024
    Article
  19. Article
  20. Article

134 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Sudheer K MantenaCenter for Free Radical Biology, Department of Environmental Health Sciences, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Adrienne L King
Kelly K Andringa
Heather B Eccleston
Shannon M Bailey
University of Alabama at Birmingham · US

Funding

Redox Modification of Thiols in Alcohol HepatotoxicityR01AA015172 · NIAAA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BAILEY, SHANNON MARIE · 2004 to 2008
$1.4M
Proteomics of Oxidant-Induced Mitochondrial Damage in an Animal Model of NASHR21DK073775 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BAILEY, SHANNON MARIE · 2006 to 2007
$395k
NIAAA NIH HHS AA15172NIAAA NIH HHS R01 AA015172NIDDK NIH HHS DK73775NIDDK NIH HHS R21 DK073775
6 · The paper itself

Abstract

Fatty liver disease associated with chronic alcohol consumption or obesity/type 2 diabetes has emerged as a serious public health problem. Steatosis, accumulation of triglyceride in hepatocytes, is now recognized as a critical "first-hit" in the pathogenesis of liver disease. It is proposed that steatosis "primes" the liver to progress to more severe liver pathologies when individuals are exposed to subsequent metabolic and/or environmental stressors or "second-hits." Genetic risk factors can also influence the susceptibility to and severity of fatty liver disease. Furthermore, oxidative stress, disrupted nitric oxide (NO) signaling, and mitochondrial dysfunction are proposed to be key molecular events that accelerate or worsen steatosis and initiate progression to steatohepatitis and fibrosis. This review article will discuss the following topics regarding the pathobiology and molecular mechanisms responsible for fatty liver disease: (1) the "two-hit" or "multi-hit" hypothesis, (2) the role of mitochondrial bioenergetic defects and oxidant stress, (3) the interplay between NO and mitochondria in fatty liver disease, (4) genetic risk factors and oxidative stress-responsive genes, and (5) the feasibility of antioxidants for treatment.

Indexed as

Oxidative StressAlcoholsAnimalsAntioxidantsDisease ProgressionFatty AcidsFatty LiverFibrosisFree RadicalsHepatocytesHumansMitochondriaModels, BiologicalObesityProteomicsAlcoholsAntioxidantsFatty AcidsFree Radicals

Identifiers

PMID18242193
PMCPMC2323912
OpenAlexW1977194186

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.