ArticleAutophagy2012
Autophagy is a protective response to ethanol neurotoxicity.
Article in Autophagy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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Who cites it
98 citing papers in PubMed, 160 citations in OpenAlex.
- Prenatal Alcohol Exposure and Mitochondrial Function in the Brain.Advances in experimental medicine and biology · 2026Review
- Impact of Prenatal Alcohol Exposure on the Cerebral Circulation: Potential Implications for Stroke.Advances in experimental medicine and biology · 2026Review
- Neurotoxicity of Chronic Alcohol Exposure: Mechanistic Insights, Cellular Disruption, and Emerging Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Astaxanthin reverses neurodevelopmental impairment by decreasing oxidative stress-induced disruption of Maf/Bcl2 signaling in prenatal alcohol exposure.Neuroreport · 2025Article
- Roles of Oxidative Stress and Autophagy in Alcohol-Mediated Brain Damage.Antioxidants (Basel, Switzerland) · 2025Review
- Evaluation of TRPM2 Channel-Mediated Autophagic Signaling Pathway in Hippocampus and Cortex Tissues of Rat Offspring Following Prenatal Exposure to Elevated Alcohol Levels.Environmental toxicology · 2025Article
- Experimental and clinical tests of FDA-approved kinase inhibitors for the treatment of neurological disorders (update 2024).Exploration of drug science · 2025Article
- Navigating redox imbalance: the role of oxidative stress in embryonic development and long-term health outcomes.Frontiers in cell and developmental biology · 2025Review
- Alcohol induces p53-mediated apoptosis in neural crest by stimulating an AMPK-mediated suppression of TORC1, S6K, and ribosomal biogenesis.Reproductive toxicology (Elmsford, N.Y.) · 2024Article
- Quercetin attenuated ropivacaine-induced neurotoxicity in SH-SY5Y cells through upregulating Pim1 and enhancing autophagy.Heliyon · 2024Article
- Enhanced autophagy and phagocytosis of apoptotic lymphocytes in splenic macrophages of acute ethanol-treated rats: Light and electron microscopic studies.Histology and histopathology · 2024Article
- An overview of current advances in perinatal alcohol exposure and pathogenesis of fetal alcohol spectrum disorders.Journal of neurodevelopmental disorders · 2024Review
- Zebrafish raptor mutation inhibits the activity of mTORC1, inducing craniofacial defects due to autophagy-induced neural crest cell death.Development (Cambridge, England) · 2024Article
- Article
- Activation of STING signaling aggravates chronic alcohol exposure-induced cognitive impairment by increasing neuroinflammation and mitochondrial apoptosis.CNS neuroscience & therapeutics · 2024Article
- Alcohol exposure suppresses ribosome biogenesis and causes nucleolar stress in cranial neural crest cells.PloS one · 2024Article
- Ameliorative effect of diazepam against ethanol-induced mitochondrial disruption in brains of the mice.Toxicology reports · 2023Article
- 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 · 2023Review
- The dual role of autophagy in periprosthetic osteolysis.Frontiers in cell and developmental biology · 2023Review
- NF-κB1 p50 stabilizes HIF-1α protein through suppression of ATG7-dependent autophagy.Cell death & disease · 2022Article
38 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Ethanol is a neuroteratogen and neurodegeneration is the most devastating consequence of developmental exposure to ethanol. The mechanisms underlying ethanol-induced neurodegeneration are complex. Ethanol exposure produces reactive oxygen species (ROS) which cause oxidative stress in the brain. We hypothesized that ethanol would activate autophagy to alleviate oxidative stress and neurotoxicity. Our results indicated that ethanol increased the level of the autophagic marker Map1lc3-II (LC3-II) and upregulated LC3 puncta in SH-SY5Y neuroblastoma cells. It also enhanced the levels of LC3-II and BECN1 in the developing brain; meanwhile, ethanol reduced SQSTM1 (p62) levels. Bafilomycin A(1), an inhibitor of autophagosome and lysosome fusion, increased p62 levels in the presence of ethanol. Bafilomycin A(1) and rapamycin potentiated ethanol-increased LC3 lipidation, whereas wortmannin and a BECN1-specific shRNA inhibited ethanol-promoted LC3 lipidation. Ethanol increased mitophagy, which was also modulated by BECN1 shRNA and rapamycin. The evidence suggested that ethanol promoted autophagic flux. Activation of autophagy by rapamycin reduced ethanol-induced ROS generation and ameliorated ethanol-induced neuronal death in vitro and in the developing brain, whereas inhibition of autophagy by wortmannin and BECN1-specific shRNA potentiated ethanol-induced ROS production and exacerbated ethanol neurotoxicity. Furthermore, ethanol inhibited the MTOR pathway and downregulation of MTOR offered neuroprotection. Taken together, the results suggest that autophagy activation is a neuroprotective response to alleviate ethanol toxicity. Ethanol modulation of autophagic activity may be mediated by the MTOR pathway.
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Registered trials
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.