Evidence map›Paper›PMID 20362583›Full record

ArticleJournal of molecular and cellular cardiology2010

Aldehyde dehydrogenase 2 knockout accentuates ethanol-induced cardiac depression: role of protein phosphatases.

Heng Ma, Lu Yu, Emily A Byra, Nan Hu, Kyoko Kitagawa, Keiichi I Nakayama, Toshihiro Kawamoto, Jun Ren

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

43 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. HostFrontiers in microbiology · 2025
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  19. Etiology of alcoholic cardiomyopathy: Mitochondria, oxidative stress and apoptosis.The international journal of biochemistry & cell biology · 2017
    Review
  20. Review
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

8 authors at 5 institutions in 3 countries.

Heng MaDepartment of Physiology, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032 China.
Lu Yu
Emily A Byra
Nan Hu
Kyoko Kitagawa
Keiichi I Nakayama
Toshihiro Kawamoto
Jun Ren
University of Wyoming · USAir Force Medical University · CNHamamatsu University School of Medicine · JPKyushu University · JPUniversity of Occupational and Environmental Health Japan · JP

Funding

Role of Acetaldehyde in Alcoholic CardiomyopathyR01AA013412 · NIAAA · UNIVERSITY OF WYOMING · PI REN, JUN · 2004 to 2008
$1.0M
NIAAA NIH HHS 1R01 AA013412NIAAA NIH HHS R01 AA013412
6 · The paper itself

Abstract

Alcohol consumption leads to myocardial contractile dysfunction possibly due to the toxicity of ethanol and its major metabolite acetaldehyde. This study was designed to examine the influence of mitochondrial aldehyde dehydrogenase-2 (ALDH2) knockout (KO) on acute ethanol exposure-induced cardiomyocyte dysfunction. Wild-type (WT) and ALDH2 KO mice were subjected to acute ethanol (3g/kg, i.p.) challenge and cardiomyocyte contractile function was assessed 24h later using an IonOptix edge detection system. Western blot analysis was performed to evaluate ALDH2, protein phosphatase 2A (PP2A), phosphorylation of Akt, and glycogen synthase kinase-3beta (GSK-3beta). ALDH2 KO accentuated ethanol-induced elevation in cardiac acetaldehyde levels. Ethanol exposure depressed cardiomyocyte contractile function including decreased cell shortening amplitude and maximal velocity of shortening/relengthening as well as prolonged relengthening duration and a greater decline in peak shortening in response to increasing stimulus frequency, the effect of which was significantly exaggerated by ALDH2 KO. ALDH2 KO also unmasked an ethanol-induced prolongation of shortening duration. In addition, short-term in vitro incubation of ethanol-induced cardiomyocyte mechanical defects was exacerbated by the ALDH inhibitor cyanamide. Ethanol treatment dampened phosphorylation of Akt and GSK-3beta associated with upregulated PP2A, which was accentuated by ALDH2 KO. ALDH2 KO aggravated ethanol-induced decrease in mitochondrial membrane potential. These results suggested that ALDH2 deficiency led to worsened ethanol-induced cardiomyocyte function, possibly due to upregulated expression of protein phosphatase, depressed Akt activation, and subsequently impaired mitochondrial function. These findings depict a critical role of ALDH2 in the pathogenesis of alcoholic cardiomyopathy.

Indexed as

Aldehyde DehydrogenaseAldehyde Dehydrogenase, MitochondrialAnimalsBiomechanical PhenomenaEnvironmental ExposureEthanolGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaMembrane Potential, MitochondrialMiceMice, Inbred C57BLMice, KnockoutMitochondriaMyocardiumMyocytes, CardiacPhosphorylationAldehyde DehydrogenaseAldehyde Dehydrogenase, MitochondrialALDH2 protein, mouseEthanolGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, mouseProtein Phosphatase 2Proto-Oncogene Proteins c-akt

Identifiers

PMID20362583
PMCPMC2885537
OpenAlexW2131175598

What OpenQuestion holds

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LicenceTDM
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.