Evidence map›Paper›PMID 20651005›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2010

Chronic ethanol consumption enhances sensitivity to Ca(2+)-mediated opening of the mitochondrial permeability transition pore and increases cyclophilin D in liver.

Adrienne L King, Telisha M Swain, Dale A Dickinson, Mathieu J Lesort, Shannon M Bailey

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Mitochondrial Calcium Signaling in Hepatocyte Health and Disease.Cold Spring Harbor perspectives in biology · 2026
    Review
  3. Review
  4. Enhanced CaNature communications · 2023
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Involvement of the mitochondrial permeability transition pore in chronic ethanol-mediated liver injury in mice.American journal of physiology. Gastrointestinal and liver physiology · 2014
    Article
  12. Article
  13. Role of Mitochondria in Alcoholic Liver Disease.Current pathobiology reports · 2013
    Article
  14. Article
  15. Article
  16. Article
  17. Article
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.

Adrienne L KingDept. of Environmental Health Sciences, Center for Free Radical Biology, Univ. of Alabama at Birmingham, AL 35294, USA.
Telisha M Swain
Dale A Dickinson
Mathieu J Lesort
Shannon M Bailey
University of Alabama at Birmingham · US

Funding

Alcoholic Liver Dysfunction Potentiation by Hyperlipidemia and Cigarette SmokeR01AA018841 · NIAAA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BAILEY, SHANNON MARIE · 2009 to 2013
$1.5M
Redox Modification of Thiols in Alcohol HepatotoxicityR01AA015172 · NIAAA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BAILEY, SHANNON MARIE · 2004 to 2008
$1.4M
NIAAA NIH HHS AA-15172NIAAA NIH HHS AA-18841NIAAA NIH HHS R01 AA015172NIAAA NIH HHS R01 AA018841
6 · The paper itself

Abstract

Chronic ethanol consumption increases mitochondrial oxidative stress and sensitivity to form the mitochondrial permeability transition pore (MPTP). The mechanism responsible for increased MPTP sensitivity in ethanol-exposed mitochondria and its relation to mitochondrial Ca(2+) handling is unknown. Herein, we investigated whether increased sensitivity to MPTP induction in liver mitochondria from ethanol-fed rats compared with controls is related to an ethanol-dependent change in mitochondrial Ca(2+) accumulation. Liver mitochondria were isolated from control and ethanol-fed rats, and Ca(2+)-mediated induction of the MPTP and mitochondrial Ca(2+) retention capacity were measured. Levels of proposed MPTP proteins as well as select pro- and antiapoptotic proteins were measured along with gene expression. We observed increased steatosis and TUNEL-stained nuclei in liver of ethanol-fed rats compared with controls. Liver mitochondria from ethanol-fed rats had increased levels of proapoptotic Bax protein and reduced Ca(2+) retention capacity compared with control mitochondria. We observed increased cyclophilin D (Cyp D) gene expression in liver and protein in mitochondria from ethanol-fed animals compared with controls, whereas there was no change in the adenine nucleotide translocase and voltage-dependent anion channel. Together, these results suggest that enhanced sensitivity to Ca(2+)-mediated MPTP induction may be due, in part, to higher Cyp D levels in liver mitochondria from ethanol-fed rats. Therefore, therapeutic strategies aimed at normalizing Cyp D levels may be beneficial in preventing ethanol-dependent mitochondrial dysfunction and liver injury.

Indexed as

AnimalsCalciumCyclophilinsEthanolGene Expression RegulationLiverMaleMitochondria, LiverMitochondrial MembranesMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PorePeptidyl-Prolyl Isomerase FPermeabilityRatsRats, Sprague-DawleyCalciumCyclophilinsEthanolMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PorePeptidyl-Prolyl Isomerase F

Identifiers

PMID20651005
PMCPMC2957342
OpenAlexW2103141671

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.