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甲基苯丙胺诱导的神经元损伤中程序性细胞死亡的分子机制。

Molecular mechanisms of programmed cell death in methamphetamine-induced neuronal damage.

作者信息

Guo Dongming, Huang Xinlei, Xiong Tianqing, Wang Xingyi, Zhang Jingwen, Wang Yingge, Liang Jingyan

机构信息

Institute of Translational Medicine, Medical, Yangzhou University, Yangzhou, China.

Department of Neurology, Affiliated Hospital of Yangzhou University, Yangzhou, China.

出版信息

Front Pharmacol. 2022 Aug 17;13:980340. doi: 10.3389/fphar.2022.980340. eCollection 2022.

Abstract

Methamphetamine, commonly referred to as METH, is a highly addictive psychostimulant and one of the most commonly misused drugs on the planet. Using METH continuously can increase your risk for drug addiction, along with other health complications like attention deficit disorder, memory loss, and cognitive decline. Neurotoxicity caused by METH is thought to play a significant role in the onset of these neurological complications. The molecular mechanisms responsible for METH-caused neuronal damage are discussed in this review. According to our analysis, METH is closely associated with programmed cell death (PCD) in the process that causes neuronal impairment, such as apoptosis, autophagy, necroptosis, pyroptosis, and ferroptosis. In reviewing this article, some insights are gained into how METH addiction is accompanied by cell death and may help to identify potential therapeutic targets for the neurological impairment caused by METH abuse.

摘要

甲基苯丙胺,通常简称为冰毒,是一种极易上瘾的精神兴奋剂,也是全球最常被滥用的毒品之一。持续使用冰毒会增加成瘾风险,还会引发其他健康问题,如注意力缺陷障碍、记忆力减退和认知能力下降。冰毒导致的神经毒性被认为在这些神经并发症的发生中起重要作用。本综述讨论了导致冰毒所致神经元损伤的分子机制。根据我们的分析,在导致神经元损伤的过程中,冰毒与程序性细胞死亡(PCD)密切相关,如凋亡、自噬、坏死性凋亡、炎性小体介导的细胞焦亡和铁死亡。通过对本文的综述,我们对冰毒成瘾如何伴随细胞死亡有了一些认识,这可能有助于确定冰毒滥用所致神经损伤的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97ac/9428134/d47c3aae38cd/fphar-13-980340-g001.jpg

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