Evidence map›Paper›PMID 25484085›Full record

ReviewAutophagy2014

Autophagy and ethanol neurotoxicity.

Jia Luo

Open access · bronzeAbstract readReview
In one paragraph

Review in Autophagy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.

  1. Pooled it
  2. Prenatal Alcohol Exposure and Mitochondrial Function in the Brain.Advances in experimental medicine and biology · 2026
    Review
  3. Review
  4. Article
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  7. Article
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  18. Maximakinin reduced intracellular CaHypertension research : official journal of the Japanese Society of Hypertension · 2023
    Article
  19. Article
  20. A multi-organ analysis of the role of mTOR in fetal alcohol spectrum disorders.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Review

17 more citing papers are in PubMed but not listed here.

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.

Jia Luoa Department of Pharmacology and Nutritional Sciences ; University of Kentucky College of Medicine ; Lexington , KY USA.
University of Kentucky · US

Funding

GSK3BETA, A MEDIATOR OF ETHANOL NEUROTOXICITYR01AA015407 · NIAAA · WEST VIRGINIA UNIVERSITY · PI JIA LUO · 2005 to 2026
$6.2M
Autophagic Protection of Ethanol NeurotoxicityR21AA019693 · NIAAA · UNIVERSITY OF KENTUCKY · PI LUO, JIA · 2010 to 2011
$392k
Thiamine deficiency and alcohol-induced neurodegenerationI01BX001721 · VA · VA MEDICAL CENTER - LEXINGTON, KY · PI LUO, JIA · 2014 to 2022
–
BLRD VA I01 BX001721NIAAA NIH HHS AA015407NIAAA NIH HHS AA019693NIAAA NIH HHS R01 AA015407
6 · The paper itself

Abstract

Excessive ethanol exposure is detrimental to the brain. The developing brain is particularly vulnerable to ethanol such that prenatal ethanol exposure causes fetal alcohol spectrum disorders (FASD). Neuronal loss in the brain is the most devastating consequence and is associated with mental retardation and other behavioral deficits observed in FASD. Since alcohol consumption during pregnancy has not declined, it is imperative to elucidate the underlying mechanisms and develop effective therapeutic strategies. One cellular mechanism that acts as a protective response for the central nervous system (CNS) is autophagy. Autophagy regulates lysosomal turnover of organelles and proteins within cells, and is involved in cell differentiation, survival, metabolism, and immunity. We have recently shown that ethanol activates autophagy in the developing brain. The autophagic preconditioning alleviates ethanol-induced neuron apoptosis, whereas inhibition of autophagy potentiates ethanol-stimulated reactive oxygen species (ROS) and exacerbates ethanol-induced neuroapoptosis. The expression of genes encoding proteins required for autophagy in the CNS is developmentally regulated; their levels are much lower during an ethanol-sensitive period than during an ethanol-resistant period. Ethanol may stimulate autophagy through multiple mechanisms; these include induction of oxidative stress and endoplasmic reticulum stress, modulation of MTOR and AMPK signaling, alterations in BCL2 family proteins, and disruption of intracellular calcium (Ca2+) homeostasis. This review discusses the most recent evidence regarding the involvement of autophagy in ethanol-mediated neurotoxicity as well as the potential therapeutic approach of targeting autophagic pathways.

Indexed as

AnimalsApoptosisAutophagyBrainEthanolHumansNeuronsReactive Oxygen SpeciesEthanolReactive Oxygen SpeciesAD, Alzheimer diseasealcoholalcoholismALS, autophagy-lysosome systemAMPK, adenosine 5′-monophosphate-activated protein kinase;ATG, autophagy-relatedCNS, central nervous systemdevelopmentER, endoplasmic reticulumFASD, fetal alcohol spectrum disordersfetal alcohol spectrum disordersFOXO3, forkhead box O3GSK3B, glycogen synthase kinase 3 βHD, Huntington disease, HNSCs, hippocampal neural stem cellsLC3, microtubule-associated protein 1 light chain 3MTORC1, MTOR complex 1MTOR, mechanistic target of rapamycin (serine/threonine kinase)neurodegenerationNFE2L2, nuclear factor, erythroid 2-like 2NOX, NADPH oxidaseoxidative stressPD, Parkinson diseasePI3K, class I phosphoinositide 3-kinaseprotein degradationROS, reactive oxygen speciesSQSTM1/p62, sequestosome 1TSC1/2, tuberous sclerosis 1/ 2UPR, unfolded protein response

Identifiers

PMID25484085
PMCPMC4502825
OpenAlexW2066119887

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.