Modulation of autophagy by melatonin and its receptors: implications in brain disorders.

IF 6.9 1区 医学 Q1 CHEMISTRY, MULTIDISCIPLINARY Acta Pharmacologica Sinica Pub Date : 2024-10-24 DOI:10.1038/s41401-024-01398-2
Chen-Ze Zhu, Gui-Zhi Li, Hai-Feng Lyu, Yang-Yang Lu, Yue Li, Xiang-Nan Zhang
{"title":"Modulation of autophagy by melatonin and its receptors: implications in brain disorders.","authors":"Chen-Ze Zhu, Gui-Zhi Li, Hai-Feng Lyu, Yang-Yang Lu, Yue Li, Xiang-Nan Zhang","doi":"10.1038/s41401-024-01398-2","DOIUrl":null,"url":null,"abstract":"<p><p>Autophagy plays a crucial role in maintaining neuronal homeostasis and function, and its disruption is linked to various brain diseases. Melatonin, an endogenous hormone that primarily acts through MT1 and MT2 receptors, regulates autophagy via multiple pathways. Growing evidence indicates that melatonin's ability to modulate autophagy provides therapeutic and preventive benefits in brain disorders, including neurodegenerative and affective diseases. In this review, we summarize the key mechanisms by which melatonin affects autophagy and explore its therapeutic potential in the treatment of brain disorders.</p>","PeriodicalId":6942,"journal":{"name":"Acta Pharmacologica Sinica","volume":" ","pages":""},"PeriodicalIF":6.9000,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta Pharmacologica Sinica","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41401-024-01398-2","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CHEMISTRY, MULTIDISCIPLINARY","Score":null,"Total":0}
引用次数: 0

Abstract

Autophagy plays a crucial role in maintaining neuronal homeostasis and function, and its disruption is linked to various brain diseases. Melatonin, an endogenous hormone that primarily acts through MT1 and MT2 receptors, regulates autophagy via multiple pathways. Growing evidence indicates that melatonin's ability to modulate autophagy provides therapeutic and preventive benefits in brain disorders, including neurodegenerative and affective diseases. In this review, we summarize the key mechanisms by which melatonin affects autophagy and explore its therapeutic potential in the treatment of brain disorders.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
褪黑激素及其受体对自噬的调节:对脑部疾病的影响。
自噬在维持神经元稳态和功能方面发挥着至关重要的作用,自噬的破坏与各种脑部疾病有关。褪黑素是一种内源性激素,主要通过 MT1 和 MT2 受体发挥作用,通过多种途径调节自噬。越来越多的证据表明,褪黑激素调节自噬的能力可治疗和预防脑部疾病,包括神经退行性疾病和情感性疾病。在这篇综述中,我们总结了褪黑激素影响自噬的主要机制,并探讨了它在治疗脑部疾病方面的治疗潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Acta Pharmacologica Sinica
Acta Pharmacologica Sinica 医学-化学综合
CiteScore
15.10
自引率
2.40%
发文量
4365
审稿时长
2 months
期刊介绍: APS (Acta Pharmacologica Sinica) welcomes submissions from diverse areas of pharmacology and the life sciences. While we encourage contributions across a broad spectrum, topics of particular interest include, but are not limited to: anticancer pharmacology, cardiovascular and pulmonary pharmacology, clinical pharmacology, drug discovery, gastrointestinal and hepatic pharmacology, genitourinary, renal, and endocrine pharmacology, immunopharmacology and inflammation, molecular and cellular pharmacology, neuropharmacology, pharmaceutics, and pharmacokinetics. Join us in sharing your research and insights in pharmacology and the life sciences.
期刊最新文献
Publisher Correction: E3 ubiquitin ligase UBR5 modulates circadian rhythm by facilitating the ubiquitination and degradation of the key clock transcription factor BMAL1. Trametinib, an anti-tumor drug, promotes oligodendrocytes generation and myelin formation. Ginsenoside Rg1 mitigates cerebral ischaemia/reperfusion injury in mice by inhibiting autophagy through activation of mTOR signalling. Oncoprotein LAMTOR5-mediated CHOP silence via DNA hypermethylation and miR-182/miR-769 in promotion of liver cancer growth. ErbB4 deficiency exacerbates olfactory dysfunction in an early-stage Alzheimer's disease mouse model.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1