{"title":"Molecular mechanism of programmed cell death in drug-induced neuronal damage: A special focus on ketamine-induced neurotoxicity","authors":"Peipei Wang , Tong Niu , Degao Huang, Yuanlong Li, Zihan Jiang, Xia Wang, Linchuan Liao","doi":"10.1016/j.tox.2025.154102","DOIUrl":null,"url":null,"abstract":"<div><div>In recent years, the abuse of ketamine as a recreational drug has been growing, and has become one of the most widely abused drugs. Continuous using ketamine poses a risk of drug addiction and complications such as attention deficit disorder, memory loss and cognitive decline. Ketamine-induced neurotoxicity is thought to play a key role in the development of these neurological complications. In this paper, we focus on the molecular mechanisms of ketamine-induced neurotoxicity. According to our analyses, drugs in causing neurotoxicity are closely associated with programmed cell death (PCD) such as apoptosis, autophagy, necroptosis, pyroptosis, and Ferroptosis. Therefore, this review will collate the existing mechanisms of programmed death in ketamine-induced neurotoxicity as well as explore the possible mechanisms by outlining the mechanisms of programmed death in other drug-induced neurotoxicity, which may be helpful in identifying potential therapeutic targets for neurotoxicity induced by ketamine abuse.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"513 ","pages":"Article 154102"},"PeriodicalIF":4.8000,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxicology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0300483X25000587","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"PHARMACOLOGY & PHARMACY","Score":null,"Total":0}
引用次数: 0
Abstract
In recent years, the abuse of ketamine as a recreational drug has been growing, and has become one of the most widely abused drugs. Continuous using ketamine poses a risk of drug addiction and complications such as attention deficit disorder, memory loss and cognitive decline. Ketamine-induced neurotoxicity is thought to play a key role in the development of these neurological complications. In this paper, we focus on the molecular mechanisms of ketamine-induced neurotoxicity. According to our analyses, drugs in causing neurotoxicity are closely associated with programmed cell death (PCD) such as apoptosis, autophagy, necroptosis, pyroptosis, and Ferroptosis. Therefore, this review will collate the existing mechanisms of programmed death in ketamine-induced neurotoxicity as well as explore the possible mechanisms by outlining the mechanisms of programmed death in other drug-induced neurotoxicity, which may be helpful in identifying potential therapeutic targets for neurotoxicity induced by ketamine abuse.
期刊介绍:
Toxicology is an international, peer-reviewed journal that publishes only the highest quality original scientific research and critical reviews describing hypothesis-based investigations into mechanisms of toxicity associated with exposures to xenobiotic chemicals, particularly as it relates to human health. In this respect "mechanisms" is defined on both the macro (e.g. physiological, biological, kinetic, species, sex, etc.) and molecular (genomic, transcriptomic, metabolic, etc.) scale. Emphasis is placed on findings that identify novel hazards and that can be extrapolated to exposures and mechanisms that are relevant to estimating human risk. Toxicology also publishes brief communications, personal commentaries and opinion articles, as well as concise expert reviews on contemporary topics. All research and review articles published in Toxicology are subject to rigorous peer review. Authors are asked to contact the Editor-in-Chief prior to submitting review articles or commentaries for consideration for publication in Toxicology.