ArticleMolecular neurobiology2022
Acetaldehyde Induces Cytotoxicity via Triggering Mitochondrial Dysfunction and Overactive Mitophagy.
Article in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Alcohol and Hypertension-A Fresh Look on the Mechanistic Aspects of a Fatal Epidemiologic Relationship.Biomolecules · 2026Review
- Mitochondrial vulnerability to aldehydic load and the role mitochondrial aldehyde dehydrogenases.Pharmacological research · 2026Review
- Age and Sex Differences in Alcohol Withdrawal Syndrome.Mayo Clinic proceedings. Innovations, quality & outcomes · 2026Article
- Challenges, optimization, and delivery strategies in the heterologous expression of aldehyde dehydrogenase: therapeutic applications for acetaldehyde detoxification.Biotechnology letters · 2026Review
- IGFBP2 Knockdown Ameliorates Diabetic Gastroparesis by Inhibiting VDAC1-Dependent Mitophagy in Interstitial Cells of CajalEndocrine, metabolic & immune disorders drug targets · 2026Article
- Bioactive Artificial Cells as Autonomous Metabolic Actuators Enable Bidirectional Communication with Tumor Cells.Journal of the American Chemical Society · 2025Article
- Synergistic toxicity in alcohol-associated liver disease and PFAS exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2025Review
- GLP-1 receptor agonism results in reduction in hepatic ethanol metabolism.npj metabolic health and disease · 2025Article
- Risk factors and clinical prediction models for short-term recurrence after endoscopic surgery in patients with colorectal polyps.World journal of gastrointestinal surgery · 2025Article
- Biological Modulation of Autophagy by Nanoplastics: A Current Overview.International journal of molecular sciences · 2025Review
- Roles of Oxidative Stress and Autophagy in Alcohol-Mediated Brain Damage.Antioxidants (Basel, Switzerland) · 2025Review
- Cyto- and Genotoxicity of Selected Plant Extracts and Microbial Metabolites with Confirmed Activity Against Phytopathogens of Potato Seed (Molecules (Basel, Switzerland) · 2025Article
- World no-tobacco: effects of second-hand smoke (SHS) and vapors on the developing and adult brain.Frontiers in pharmacology · 2025Review
- Mitochondrial metabolism: A moving target in hepatocellular carcinoma therapy.Journal of cellular physiology · 2025Review
- Study on the protective effects and mechanisms of eleutherococcus senticosus on korsakoff syndrome.Frontiers in neuroscience · 2025Review
- Astaxanthin Inhibits HMarine drugs · 2024Article
- Polystyrene nanoplastic exposure induces excessive mitophagy by activating AMPK/ULK1 pathway in differentiated SH-SY5Y cells and dopaminergic neurons in vivo.Particle and fibre toxicology · 2023Article
- Fetal alcohol spectrum disorders.Nature reviews. Disease primers · 2023Review
- Brain ethanol metabolism and mitochondria.Current topics in biochemical research · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overconsumption of alcohol damages brain tissue and causes cognitive dysfunction. It has been suggested that the neurotoxicity caused by excessive alcohol consumption is largely mediated by acetaldehyde, the most toxic metabolite of ethanol. Evidence shows that acetaldehyde impairs mitochondrial function and induces cytotoxicity of neuronal cells; however, the exact mechanisms are not fully understood. The aim of this study was to investigate the role of mitophagy in acetaldehyde-induced cytotoxicity. It was found that acetaldehyde treatment induced mitophagic responses and caused cytotoxicity in SH-SY5Y cells. The levels of light chain 3 (LC3)-II, Beclin1, autophagy-related protein (Atg) 5 and Atg16L1, PTEN-induced putative kinase (PINK)1, and Parkin were significantly elevated, while the level of p62 was reduced in acetaldehyde-treated cells. Acetaldehyde also promoted the accumulation of PINK1 and Parkin on mitochondria and caused a remarkable decrease of mitochondrial mass. Treatment with autophagy inhibitors prevented the decline of mitochondrial mass and alleviated the cytotoxicity induced by acetaldehyde, suggesting that overactive mitophagy might be an important mechanism contributing to acetaldehyde-induced cytotoxicity. Antioxidant N-acetyl-L-cysteine significantly attenuated the mitophagic responses and alleviated the cytotoxicity induced by acetaldehyde, indicating that oxidative stress was a major mediator of the excessive mitophagy induced by acetaldehyde. Taken together, these findings provided new insights into the role of mitophagy and oxidative stress in acetaldehyde-induced cytotoxicity.
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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.