• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

通过激效作用靶向与年龄相关的分子损伤的发生、消除和积累。

Targeting the age-related occurrence, removal, and accumulation of molecular damage by hormesis.

机构信息

Laboratory of Cellular Ageing, Department of Molecular Biology, Aarhus University, Aarhus, Denmark.

出版信息

Ann N Y Acad Sci. 2010 Jun;1197:28-32. doi: 10.1111/j.1749-6632.2010.05193.x.

DOI:10.1111/j.1749-6632.2010.05193.x
PMID:20536829
Abstract

Strategies for testing and developing effective means of intervention, prevention, and modulation of aging incorporate means to minimize the occurrence and accumulation of molecular damage, to reduce molecular heterogeneity, and to evaluate the relevance of the type and extent of damage with respect to its role in aging and age-related diseases. One such approach is that of mild stress-induced hormesis, which stimulates maintenance and repair systems and strengthens the homeodynamic space of cells and organisms. Hormesis through mild heat shock, natural and synthetic hormetins, and other stressors brings about several antiaging effects in human fibroblasts, keratinocytes, and telomerase-immortalized bone marrow stem cells. Depending on the cell type, these antiaging hormetic effects include extension of replicative life span, enhanced proteasomal activities, increased chaperone levels, and improved wound healing, angiogenesis, and differentiation. The main molecular pathways for achieving such hormetic effects are through targeting the processes for the repair and removal of molecular damage, which can slow aging.

摘要

测试和开发有效干预、预防和调节衰老的策略包括尽量减少分子损伤的发生和积累、减少分子异质性、评估损伤的类型和程度与衰老和与衰老相关疾病的关系的方法。其中一种方法是温和应激诱导的应激反应,它可以刺激维持和修复系统,增强细胞和生物体的内稳空间。温和热休克、天然和合成的应激素以及其他应激源引起的应激反应在人类成纤维细胞、角质细胞和端粒酶永生化骨髓干细胞中产生了几种抗衰老作用。根据细胞类型的不同,这些抗衰老应激反应包括延长复制寿命、增强蛋白酶体活性、增加伴侣蛋白水平以及改善伤口愈合、血管生成和分化。实现这种应激反应的主要分子途径是通过靶向修复和清除分子损伤的过程,这可以减缓衰老。

相似文献

1
Targeting the age-related occurrence, removal, and accumulation of molecular damage by hormesis.通过激效作用靶向与年龄相关的分子损伤的发生、消除和积累。
Ann N Y Acad Sci. 2010 Jun;1197:28-32. doi: 10.1111/j.1749-6632.2010.05193.x.
2
Hormetic prevention of molecular damage during cellular aging of human skin fibroblasts and keratinocytes.人类皮肤成纤维细胞和角质形成细胞细胞衰老过程中分子损伤的 hormetic 预防作用。
Ann N Y Acad Sci. 2007 Apr;1100:424-30. doi: 10.1196/annals.1395.047.
3
Stress-mediated hormetic modulation of aging, wound healing, and angiogenesis in human cells.应激介导的人体细胞衰老、伤口愈合和血管生成的适应性调节
Ann N Y Acad Sci. 2007 Nov;1119:112-21. doi: 10.1196/annals.1404.005.
4
Increased molecular damage and heterogeneity as the basis of aging.分子损伤增加和异质性增加是衰老的基础。
Biol Chem. 2008 Mar;389(3):267-72. doi: 10.1515/BC.2008.030.
5
Principles and practice of hormetic treatment of aging and age-related diseases.衰老及与年龄相关疾病的 hormetic 疗法的原理与实践
Hum Exp Toxicol. 2008 Feb;27(2):151-4. doi: 10.1177/0960327107083409.
6
Proteasomal oscillation during mild heat shock in aging human skin fibroblasts.衰老的人类皮肤成纤维细胞在轻度热休克期间的蛋白酶体振荡
Ann N Y Acad Sci. 2006 May;1067:224-7. doi: 10.1196/annals.1354.028.
7
Hormesis in aging.衰老中的毒物兴奋效应。
Ageing Res Rev. 2008 Jan;7(1):63-78. doi: 10.1016/j.arr.2007.03.002. Epub 2007 Aug 31.
8
MAP kinases and heat shock-induced hormesis in human fibroblasts during serial passaging in vitro.体外连续传代培养过程中人类成纤维细胞中的丝裂原活化蛋白激酶与热休克诱导的兴奋效应
Ann N Y Acad Sci. 2006 May;1067:343-8. doi: 10.1196/annals.1354.048.
9
Hormetic mechanisms of anti-aging and rejuvenating effects of repeated mild heat stress on human fibroblasts in vitro.体外反复轻度热应激对人成纤维细胞的抗衰老和回春作用的兴奋效应机制
Rejuvenation Res. 2004 Spring;7(1):40-8. doi: 10.1089/154916804323105071.
10
Mechanisms of hormesis through mild heat stress on human cells.轻度热应激对人体细胞产生兴奋效应的机制。
Ann N Y Acad Sci. 2004 Jun;1019:554-8. doi: 10.1196/annals.1297.103.

引用本文的文献

1
Heat shock proteins and hormesis in the diagnosis and treatment of neurodegenerative diseases.热休克蛋白与兴奋效应在神经退行性疾病诊断和治疗中的应用
Immun Ageing. 2015 Nov 4;12:20. doi: 10.1186/s12979-015-0046-8. eCollection 2015.
2
L-Lactate Protects Skin Fibroblasts against Aging-Associated Mitochondrial Dysfunction via Mitohormesis.L-乳酸通过线粒体应激反应保护皮肤成纤维细胞免受与衰老相关的线粒体功能障碍影响。
Oxid Med Cell Longev. 2015;2015:351698. doi: 10.1155/2015/351698. Epub 2015 Jun 10.
3
Basal level of autophagy is increased in aging human skin fibroblasts in vitro, but not in old skin.
在体外培养的衰老人类皮肤成纤维细胞中,自噬的基础水平会升高,但在老年皮肤中则不会。
PLoS One. 2015 May 7;10(5):e0126546. doi: 10.1371/journal.pone.0126546. eCollection 2015.
4
Aging is not a disease: implications for intervention.衰老并非一种疾病:对干预措施的启示。
Aging Dis. 2014 Jun 1;5(3):196-202. doi: 10.14336/AD.2014.0500196. eCollection 2014 Jun.
5
Age- and diet-associated metabolome remodeling characterizes the aging process driven by damage accumulation.与年龄和饮食相关的代谢组重塑是由损伤积累驱动的衰老过程的特征。
Elife. 2014 Apr 29;3:e02077. doi: 10.7554/eLife.02077.
6
Stress biology and aging mechanisms: toward understanding the deep connection between adaptation to stress and longevity.压力生物学与衰老机制:探索应激适应与长寿之间的深层关联。
J Gerontol A Biol Sci Med Sci. 2014 Jun;69 Suppl 1(Suppl 1):S10-6. doi: 10.1093/gerona/glu055.
7
Updating the mitochondrial free radical theory of aging: an integrated view, key aspects, and confounding concepts.更新线粒体自由基衰老理论:综合观点、关键方面和混淆概念。
Antioxid Redox Signal. 2013 Oct 20;19(12):1420-45. doi: 10.1089/ars.2012.5148. Epub 2013 Jul 3.
8
Hormesis does not make sense except in the light of TOR-driven aging.除了从TOR驱动的衰老角度来看,兴奋效应是没有意义的。
Aging (Albany NY). 2011 Nov;3(11):1051-62. doi: 10.18632/aging.100411.
9
Gadd45 proteins: relevance to aging, longevity and age-related pathologies.Gadd45 蛋白:与衰老、长寿和与年龄相关的病理相关。
Ageing Res Rev. 2012 Jan;11(1):51-66. doi: 10.1016/j.arr.2011.09.003. Epub 2011 Oct 5.