Evidence map›Paper›PMID 31067632›Full record

ReviewInternational journal of environmental research and public health2019

Fetal Cerebral Artery Mitochondrion as Target of Prenatal Alcohol Exposure.

Anna N Bukiya

Open access · goldAbstract readReview
In one paragraph

Review in International journal of environmental research and public health, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Prenatal Alcohol Exposure and Mitochondrial Function in the Brain.Advances in experimental medicine and biology · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Frontiers in neuroscience · 2023
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Fetal Alcohol Spectrum Disorders: Fixing Our Aim to Aim for the Fix.International journal of environmental research and public health · 2019
    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

1 author at 1 institution in 1 country.

Anna N BukiyaDepartment Pharmacology, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN 38163, USA. abukiya@uthsc.edu.ORCID 0000-0003-0655-2319
University of Tennessee Health Science Center · US

Funding

Fetal cerebrovascular eCB system as a target of maternal alcohol consumptionR21AA022433 · NIAAA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI BUKIYA, ANNA · 2014 to 2015
$387k
National Institute on Alcohol Abuse and Alcoholism R21 AA022433
6 · The paper itself

Abstract

Prenatal alcohol exposure results in an array of developmental abnormalities known as fetal alcohol spectrum disorders (FASDs). Despite the high prevalence of FASDs, therapeutic interventions against accidental or intended exposure of developing fetuses to alcohol are limited. This review outlines current knowledge about mitochondria in cerebral blood vessels as a potential target for anti-FASDs intervention. First, it describes the multifaceted role of mitochondria in maintaining the cerebral artery diameter as shown in adult tissue. Second, current literature on alcohol-driven damage of mitochondrial morphology and function in several fetal tissues, including liver, heart, and brain is summarized. The functional consequences of alcohol exposure in these organs include morphological enlargement of mitochondria, increased oxidative stress, and alteration of cellular respiration. These studies point to a tissue-specific effect of alcohol on mitochondrial function and a particular vulnerability of fetal mitochondria to alcohol exposure when compared to adult counterparts. Third, recent work from our group describing persistent changes in fetal baboon cerebral artery proteome following three episodes of prenatal alcohol exposure is reviewed. In conclusion, the consequences of prenatal alcohol exposure on cerebral artery mitochondria constitute an open field of investigation and, eventually, a point of therapeutic intervention against FASDs.

Indexed as

AnimalsCerebral ArteriesEthanolFemaleFetal Alcohol Spectrum DisordersFetal DevelopmentFetusHumansMaternal-Fetal ExchangeMitochondriaPregnancyEthanolalcohol in uterobasilar arteryintrauterine alcoholmaternal drinkingneurovascular unitnonhuman primate

Identifiers

PMID31067632
PMCPMC6539770
OpenAlexW2942800945

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.