Evidence map›Paper›PMID 36873619›Full record

ArticleCurrent topics in biochemical research2022

Brain ethanol metabolism and mitochondria.

Jaylyn Waddell, Mary C McKenna, Tibor Kristian

Open access · greenAbstract read
In one paragraph

Article in Current topics in biochemical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Alcohol Metabolism into Acetaldehyde in Developing Cerebral Arteries.International journal of molecular sciences · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Protective Effects and Mechanism ofInternational journal of molecular sciences · 2024
    Article
  12. Article
  13. Review
  14. 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

3 authors at 2 institutions in 1 country.

Jaylyn WaddellDepartment of Pediatrics, University of Maryland School of Medicine, 655 W. Baltimore St., Baltimore, MD 21201, USA.
Mary C McKennaDepartment of Pediatrics, University of Maryland School of Medicine, 655 W. Baltimore St., Baltimore, MD 21201, USA.
Tibor KristianVeterans Affairs Maryland Health Center System, 10 North Greene Street, Baltimore, MD 21201, USA.
University of Maryland, Baltimore · USVA Maryland Health Care System · US

Funding

Project IV- Cerebellar Function After Hypoxia-Ischemia and Precipitating InflammationP01HD085928 · NICHD · UNIVERSITY OF MARYLAND BALTIMORE · PI MCKENNA, MARY C · 2016 to 2020
$6.3M
Targeting mitochondrial Complex I in neonatal hypoxia-ischemiaR01NS122777 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI BRIAN M POLSTER, JAYLYN Waddell WADDELL · 2022 to 2026
$2.5M
Using NAD+ precursor for treatment of global cerebral ischemiaR01NS119275 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI KRISTIAN, TIBOR · 2021 to 2025
$1.9M
The role of nicotinamide mononucleotide dependent mitochondrial reactive oxygen species generation in acute brain injuryI01BX004895 · VA · BALTIMORE VA MEDICAL CENTER · PI KRISTIAN, TIBOR · 2020 to 2024
–
BLRD VA I01 BX004895NICHD NIH HHS P01 HD085928NINDS NIH HHS R01 NS119275NINDS NIH HHS R01 NS122777
6 · The paper itself

Abstract

Alcohol abuse and dependence in humans causes an extreme shift in metabolism for which the human brain is not evolutionarily prepared. Oxidation of ethanol and acetaldehyde are not regulated, making ethanol a dominating metabolic substrate that prevents the activity of enzymes from oxidizing their usual endogenous substrates. The enzymes required to oxidize ethanol across the variety of affected tissues all produce acetaldehyde which is then converted to acetate by aldehyde dehydrogenases (ALDHs). ALDHs are NAD+-dependent enzymes, and mitochondrial ALDH2 is likely the primary contributor to ethanol-derived acetaldehyde clearance in cells. Metabolism of alcohol has several adverse effects on mitochondria including increased free radical levels, hyperacetylation of mitochondrial proteins, and excessive mitochondrial fragmentation. This review discusses the role of astrocytic and neuronal mitochondria in ethanol metabolism that contributes to the acute and chronic changes in mitochondrial function and morphology, that might promote tolerance, dependence and withdrawal. We also propose potential modes of therapeutic intervention to reduce the toxicity of chronic alcohol consumption.

Indexed as

brainethanolmitochondria

Identifiers

PMID36873619
PMCPMC9980429
OpenAlexW4323295519

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.