Evidence map›Paper›PMID 21520201›Full record

ArticleHepatology (Baltimore, Md.)2011

Mitochondria-targeted ubiquinone (MitoQ) decreases ethanol-dependent micro and macro hepatosteatosis.

Balu K Chacko, Anup Srivastava, Michelle S Johnson, Gloria A Benavides, Mi Jung Chang, Yaozu Ye, Nirag Jhala, Michael P Murphy, Balaraman Kalyanaraman, Victor M Darley-Usmar

Open access · bronzeAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 2 pooled it
7.5field-weighted citation impact, top 2% 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

78 citing papers in PubMed, 2 syntheses or guidelines pooled it, 121 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Mitochondrial Calcium Signaling in Hepatocyte Health and Disease.Cold Spring Harbor perspectives in biology · 2026
    Review
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  7. Review
  8. Review
  9. Article
  10. [Research progress on the role of invariant natural killer T cells in immune-mediated liver injury].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025
    Review
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  12. Article
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18 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

10 authors at 3 institutions in 2 countries.

Balu K ChackoCenter for Free Radical Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Anup Srivastava
Michelle S Johnson
Gloria A Benavides
Mi Jung Chang
Yaozu Ye
Nirag Jhala
Michael P Murphy
Balaraman Kalyanaraman
Victor M Darley-Usmar
University of Alabama at Birmingham · USMedical College of Wisconsin · USMRC Mitochondrial Biology Unit · GB

Funding

Ethanol toxicity and NO-dependent mitochondrial damageR01AA013395 · NIAAA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DARLEY-USMAR, VICTOR M · 2002 to 2011
$2.9M
Medical Research Council MC_U105663142NIAAA NIH HHS AA013395NIAAA NIH HHS R01 AA013395
6 · The paper itself

Abstract

unlabelledChronic alcohol-induced liver disease results in inflammation, steatosis, and increased oxidative and nitrosative damage to the mitochondrion. We hypothesized that targeting an antioxidant to the mitochondria would prevent oxidative damage and attenuate the steatosis associated with alcoholic liver disease. To test this we investigated the effects of mitochondria-targeted ubiquinone (MitoQ) (5 and 25 mg/kg/day for 4 weeks) in male Sprague-Dawley rats consuming ethanol using the Lieber-DeCarli diet with pair-fed controls. Hepatic steatosis, 3-nitrotyrosine (3-NT), 4-hydroxynonenal (4-HNE), hypoxia inducible factor α (HIF1α), and the activity of the mitochondrial respiratory chain complexes were assessed. As reported previously, ethanol consumption resulted in hepatocyte ballooning, increased lipid accumulation in the form of micro and macrovesicular steatosis, and induction of cytochrome P450 2E1 (CYP2E1). MitoQ had a minor effect on the ethanol-dependent decrease in mitochondrial respiratory chain proteins and their activities; however, it did decrease hepatic steatosis in ethanol-consuming animals and prevented the ethanol-induced formation of 3-NT and 4-HNE. Interestingly, MitoQ completely blocked the increase in HIF1α in all ethanol-fed groups, which has previously been demonstrated in cell culture models and shown to be essential in ethanol-dependent hepatosteatosis.

conclusionThese results demonstrate the antioxidant capacity of MitoQ in alleviating alcohol-associated mitochondrial reactive oxygen species (ROS) and several downstream effects of ROS/RNS (reactive nitrogen species) production such as inhibiting protein nitration and protein aldehyde formation and specifically ROS-dependent HIF1α stabilization.

Indexed as

AMP-Activated Protein KinasesAnimalsAntioxidantsCytochrome P-450 CYP2E1Disease Models, AnimalDose-Response Relationship, DrugElectron TransportEthanolFatty LiverHypoxia-Inducible Factor 1, alpha SubunitLipid MetabolismLiverMaleMitochondria, LiverOrganophosphorus CompoundsRatsAMP-Activated Protein KinasesAntioxidantsCytochrome P-450 CYP2E1EthanolHif1a protein, ratHypoxia-Inducible Factor 1, alpha SubunitmitoquinoneOrganophosphorus CompoundsReactive Oxygen SpeciesUbiquinone

Identifiers

PMID21520201
PMCPMC3125473
OpenAlexW2043429649

What OpenQuestion holds

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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.