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衰老的治疗性干预:让老方法焕发新活力并探索新策略。

Therapeutic Manipulation of Ageing: Repurposing Old Dogs and Discovering New Tricks.

作者信息

Mallikarjun Venkatesh, Swift Joe

机构信息

Wellcome Trust Centre for Cell-Matrix Research, Division of Cell Matrix Biology and Regenerative Medicine, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PT, United Kingdom..

出版信息

EBioMedicine. 2016 Dec;14:24-31. doi: 10.1016/j.ebiom.2016.11.020. Epub 2016 Nov 21.


DOI:10.1016/j.ebiom.2016.11.020
PMID:27889480
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5161440/
Abstract

Ageing is a leading risk factor for many debilitating diseases. While age-related diseases have been the subject of over a century of intense investigation, until recently, physiological ageing was considered unavoidable. Pharmacological and genetic studies have since shown that ageing is a malleable process and that its abrogation can prevent its associated diseases. This review summarises a sample of the most promising efforts to deliver the products of ageing research to the clinic. Current efforts include the use of clinically approved drugs that have since been repurposed, as well as the development of novel therapeutics, to target ageing. Furthermore, ongoing research has sought reliable biomarkers of ageing that will accelerate the development of such therapeutics. Development of these technologies will improve quality of late-life and help relieve the enormous stress placed on state healthcare systems by a rapidly ageing global population. Thus, for both medical and socioeconomic reasons, it is imperative that ageing is made to yield to intervention.

摘要

衰老 是许多使人衰弱的疾病的主要风险因素。虽然与年龄相关的疾病 已经成为一个多世纪以来深入研究的主题,但直到最近,生理衰老 仍被认为是不可避免的。从那时起,药理学和遗传学研究表明,衰老是一个可塑的过程,消除衰老可以预防其相关疾病。本综述总结了将衰老研究成果应用于临床的一些最有前景的努力。目前的努力包括使用后来被重新利用的临床批准药物,以及开发针对衰老的新型疗法。此外,正在进行的研究一直在寻找可靠的衰老生物标志物,这将加速此类疗法的开发。这些技术的发展将提高晚年生活质量,并有助于缓解全球人口迅速老龄化给国家医疗系统带来的巨大压力。因此,出于医学和社会经济原因,必须使衰老能够接受干预。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81eb/5161440/b4b1797128ef/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81eb/5161440/8149b6b4c201/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81eb/5161440/40cfda91c1f1/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81eb/5161440/da66d2495c09/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81eb/5161440/b4b1797128ef/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81eb/5161440/8149b6b4c201/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81eb/5161440/40cfda91c1f1/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81eb/5161440/da66d2495c09/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81eb/5161440/b4b1797128ef/gr3.jpg

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本文引用的文献

[1]
DNA methylation-based measures of biological age: meta-analysis predicting time to death.

Aging (Albany NY). 2016-9-28

[2]
Frameworks for Proof-of-Concept Clinical Trials of Interventions That Target Fundamental Aging Processes.

J Gerontol A Biol Sci Med Sci. 2016-11

[3]
Anti-aging pharmacology: Promises and pitfalls.

Ageing Res Rev. 2016-8-11

[4]
Metformin as a Tool to Target Aging.

Cell Metab. 2016-6-14

[5]
Keeping the senescence secretome under control: Molecular reins on the senescence-associated secretory phenotype.

Exp Gerontol. 2016-9

[6]
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Aging (Albany NY). 2016-5

[7]
Systems-level analysis of human aging genes shed new light on mechanisms of aging.

Hum Mol Genet. 2016-7-15

[8]
Comparative idiosyncrasies in life extension by reduced mTOR signalling and its distinctiveness from dietary restriction.

Aging Cell. 2016-8

[9]
Longevity-Promoting Pharmaceuticals: Is it a Time for Implementation?

Trends Pharmacol Sci. 2016-5

[10]
IL-33 ameliorates Alzheimer's disease-like pathology and cognitive decline.

Proc Natl Acad Sci U S A. 2016-5-10

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