靶向线粒体功能障碍挽救细胞衰老以治疗神经退行性疾病。

3区 生物学 Q1 Biochemistry, Genetics and Molecular Biology
Komal Sharma, Joyobrata Sarkar, Anchal Trisal, Rishika Ghosh, Anubhuti Dixit, Abhishek Kumar Singh
{"title":"靶向线粒体功能障碍挽救细胞衰老以治疗神经退行性疾病。","authors":"Komal Sharma,&nbsp;Joyobrata Sarkar,&nbsp;Anchal Trisal,&nbsp;Rishika Ghosh,&nbsp;Anubhuti Dixit,&nbsp;Abhishek Kumar Singh","doi":"10.1016/bs.apcsb.2023.02.016","DOIUrl":null,"url":null,"abstract":"<p><p>Aging is an inevitable phenomenon that causes a decline in bodily functions over time. One of the most important processes that play a role in aging is senescence. Senescence is characterized by accumulation of cells that are no longer functional but elude the apoptotic pathway. These cells secrete inflammatory molecules that comprise the senescence associated secretory phenotype (SASP). Several essential molecules such as p53, Rb, and p16INK4a regulate the senescence process. Mitochondrial regulation has been found to play an important role in senescence. Reactive oxygen species (ROS) generated from mitochondria can affect cellular senescence by inducing the persistent DNA damage response, thus stabilizing the senescence. Evidently, senescence plays a major contributory role to the development of age-related neurological disorders. In this chapter, we discuss the role of senescence in the progression and onset of several neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. Moreover, we also discuss the efficacy of certain molecules like MitoQ, SkQ1, and Latrepirdine that could be proven therapeutics with respect to these disorders by regulating mitochondrial activity.</p>","PeriodicalId":7376,"journal":{"name":"Advances in protein chemistry and structural biology","volume":"136 ","pages":"309-337"},"PeriodicalIF":0.0000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Targeting mitochondrial dysfunction to salvage cellular senescence for managing neurodegeneration.\",\"authors\":\"Komal Sharma,&nbsp;Joyobrata Sarkar,&nbsp;Anchal Trisal,&nbsp;Rishika Ghosh,&nbsp;Anubhuti Dixit,&nbsp;Abhishek Kumar Singh\",\"doi\":\"10.1016/bs.apcsb.2023.02.016\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Aging is an inevitable phenomenon that causes a decline in bodily functions over time. One of the most important processes that play a role in aging is senescence. Senescence is characterized by accumulation of cells that are no longer functional but elude the apoptotic pathway. These cells secrete inflammatory molecules that comprise the senescence associated secretory phenotype (SASP). Several essential molecules such as p53, Rb, and p16INK4a regulate the senescence process. Mitochondrial regulation has been found to play an important role in senescence. Reactive oxygen species (ROS) generated from mitochondria can affect cellular senescence by inducing the persistent DNA damage response, thus stabilizing the senescence. Evidently, senescence plays a major contributory role to the development of age-related neurological disorders. In this chapter, we discuss the role of senescence in the progression and onset of several neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. Moreover, we also discuss the efficacy of certain molecules like MitoQ, SkQ1, and Latrepirdine that could be proven therapeutics with respect to these disorders by regulating mitochondrial activity.</p>\",\"PeriodicalId\":7376,\"journal\":{\"name\":\"Advances in protein chemistry and structural biology\",\"volume\":\"136 \",\"pages\":\"309-337\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Advances in protein chemistry and structural biology\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1016/bs.apcsb.2023.02.016\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"Biochemistry, Genetics and Molecular Biology\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advances in protein chemistry and structural biology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1016/bs.apcsb.2023.02.016","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
引用次数: 0

摘要

衰老是一种不可避免的现象,它会导致身体机能随着时间的推移而下降。在衰老过程中起作用的最重要的过程之一是衰老。衰老的特征是细胞的积累,不再具有功能,但逃避凋亡途径。这些细胞分泌炎症分子,包括衰老相关分泌表型(SASP)。一些重要分子如p53、Rb和p16INK4a调节衰老过程。线粒体调控已被发现在衰老中起重要作用。线粒体产生的活性氧(Reactive oxygen species, ROS)可以通过诱导持续的DNA损伤反应来影响细胞衰老,从而稳定衰老。显然,衰老在与年龄相关的神经系统疾病的发展中起着重要的作用。在本章中,我们讨论衰老在一些神经退行性疾病的进展和发病中的作用,包括阿尔茨海默病、帕金森病、亨廷顿病和肌萎缩性侧索硬化症。此外,我们还讨论了某些分子如MitoQ、SkQ1和Latrepirdine的功效,这些分子可以通过调节线粒体活性来证明治疗这些疾病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Targeting mitochondrial dysfunction to salvage cellular senescence for managing neurodegeneration.

Aging is an inevitable phenomenon that causes a decline in bodily functions over time. One of the most important processes that play a role in aging is senescence. Senescence is characterized by accumulation of cells that are no longer functional but elude the apoptotic pathway. These cells secrete inflammatory molecules that comprise the senescence associated secretory phenotype (SASP). Several essential molecules such as p53, Rb, and p16INK4a regulate the senescence process. Mitochondrial regulation has been found to play an important role in senescence. Reactive oxygen species (ROS) generated from mitochondria can affect cellular senescence by inducing the persistent DNA damage response, thus stabilizing the senescence. Evidently, senescence plays a major contributory role to the development of age-related neurological disorders. In this chapter, we discuss the role of senescence in the progression and onset of several neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. Moreover, we also discuss the efficacy of certain molecules like MitoQ, SkQ1, and Latrepirdine that could be proven therapeutics with respect to these disorders by regulating mitochondrial activity.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Advances in protein chemistry and structural biology
Advances in protein chemistry and structural biology BIOCHEMISTRY & MOLECULAR BIOLOGY-
CiteScore
7.40
自引率
0.00%
发文量
66
审稿时长
>12 weeks
期刊介绍: Published continuously since 1944, The Advances in Protein Chemistry and Structural Biology series has been the essential resource for protein chemists. Each volume brings forth new information about protocols and analysis of proteins. Each thematically organized volume is guest edited by leading experts in a broad range of protein-related topics.
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信