Evidence map›Paper›PMID 28606389›Full record

ReviewThe international journal of biochemistry & cell biology2017

Etiology of alcoholic cardiomyopathy: Mitochondria, oxidative stress and apoptosis.

Jennifer L Steiner, Charles H Lang

Open access · greenAbstract readReview
In one paragraph

Review in The international journal of biochemistry & cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 2 pooled it
6.7field-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

58 citing papers in PubMed, 2 syntheses or guidelines pooled it, 113 citations in OpenAlex.

  1. Revisiting Secondary Dilative Cardiomyopathy.International journal of molecular sciences · 2025
    Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Prenatal Alcohol Exposure and Mitochondrial Function in the Brain.Advances in experimental medicine and biology · 2026
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Antioxidants (Basel, Switzerland) · 2025
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

2 authors at 1 institution in 1 country.

Jennifer L SteinerDepartment of Cellular and Molecular Physiology, Penn State College of Medicine, 500 University Drive, Hershey, PA 17033, United States. Electronic address: jls1075@psu.edu.
Charles H LangDepartment of Cellular and Molecular Physiology, Penn State College of Medicine, 500 University Drive, Hershey, PA 17033, United States. Electronic address: chl1@psu.edu.
Pennsylvania State University · US

Funding

Regulation of Nutrient Sensing and Muscle Wasting by AlcoholR37AA011290 · NIAAA · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI LANG, CHARLES H. · 2012 to 2021
$3.4M
Modulation of Contraction-Induced Changes in Muscle mTOR Signaling by AlcoholF32AA023422 · NIAAA · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI STEINER, JENNIFER LYNN · 2014 to 2016
$158k
NIAAA NIH HHS F32 AA023422NIAAA NIH HHS R37 AA011290
6 · The paper itself

Abstract

Putative mechanisms leading to the development of alcoholic cardiomyopathy (ACM) include the interrelated cellular processes of mitochondria metabolism, oxidative stress and apoptosis. As mitochondria fuel the constant energy demands of this continually contracting tissue, it is not surprising that alcohol-induced molecular changes in this organelle contribute to cardiac dysfunction and ACM. As the causal relationship of these processes with ACM has already been established, the primary objective of this review is to provide an update of the experimental findings to more completely understand the aforementioned mechanisms. Accordingly, recent data indicate that alcohol impairs mitochondria function assessed by membrane potential and respiratory chain activity. Indictors of oxidative stress including superoxide dismutase, glutathione metabolites and malondialdehyde are also adversely affected by alcohol oftentimes in a sex-dependent manner. Additionally, myocardial apoptosis is increased based on assessment of TUNEL staining and caspase activity. Recent work has also emerged linking alcohol-induced oxidative stress with apoptosis providing new insight on the codependence of these interrelated mechanisms in ACM. Attention is also given to methodological differences including the dose of alcohol, experimental model system and the use of males versus females to highlight inconsistencies and areas that would benefit from establishment of a consistent model.

Indexed as

ApoptosisOxidative StressAnimalsCardiomyopathy, AlcoholicHumansMitochondriaCaspaseEthanolHeartReactive oxygen speciesRespiratory chain

Identifiers

PMID28606389
PMCPMC5536333
OpenAlexW2622743229

What OpenQuestion holds

Textmetadata
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.