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本文引用的文献

1
Stability of mitochondrial membrane proteins in terrestrial vertebrates predicts aerobic capacity and longevity.线粒体膜蛋白在陆生脊椎动物中的稳定性预测其有氧能力和寿命。
Genome Biol Evol. 2011;3:1233-44. doi: 10.1093/gbe/evr079. Epub 2011 Aug 7.
2
Mitochondria: the next (neurode)generation.线粒体:下一代(神经)。
Neuron. 2011 Jun 23;70(6):1033-53. doi: 10.1016/j.neuron.2011.06.003.
3
Progerin and telomere dysfunction collaborate to trigger cellular senescence in normal human fibroblasts.早衰素与端粒功能障碍协同作用,导致正常人类成纤维细胞发生细胞衰老。
J Clin Invest. 2011 Jul;121(7):2833-44. doi: 10.1172/JCI43578. Epub 2011 Jun 13.
4
Extending life span by increasing oxidative stress.通过增加氧化应激来延长寿命。
Free Radic Biol Med. 2011 Jul 15;51(2):327-36. doi: 10.1016/j.freeradbiomed.2011.05.010. Epub 2011 May 14.
5
Successful aging and sustained good health in the naked mole rat: a long-lived mammalian model for biogerontology and biomedical research.裸鼹鼠的成功衰老与持续健康:生物老年学和生物医学研究的长寿哺乳动物模型。
ILAR J. 2011;52(1):41-53. doi: 10.1093/ilar.52.1.41.
6
Fat maintenance is a predictor of the murine lifespan response to dietary restriction.脂肪维持是饮食限制对小鼠寿命反应的预测因子。
Aging Cell. 2011 Aug;10(4):629-39. doi: 10.1111/j.1474-9726.2011.00702.x. Epub 2011 Apr 25.
7
Funding crisis hits US ageing research.资金危机冲击美国老龄化研究。
Nature. 2010 Nov 11;468(7321):148. doi: 10.1038/468148a.
8
Rapamycin, but not resveratrol or simvastatin, extends life span of genetically heterogeneous mice.雷帕霉素而非白藜芦醇或辛伐他汀可延长遗传异质性小鼠的寿命。
J Gerontol A Biol Sci Med Sci. 2011 Feb;66(2):191-201. doi: 10.1093/gerona/glq178. Epub 2010 Oct 25.
9
Highly efficient reprogramming to pluripotency and directed differentiation of human cells with synthetic modified mRNA.利用合成修饰 mRNA 高效重编程人类细胞为多能性干细胞并进行定向分化。
Cell Stem Cell. 2010 Nov 5;7(5):618-30. doi: 10.1016/j.stem.2010.08.012. Epub 2010 Sep 30.
10
Genetic variation in insulin/IGF-1 signaling pathways and longevity.胰岛素/IGF-1 信号通路的遗传变异与长寿。
Ageing Res Rev. 2011 Apr;10(2):201-4. doi: 10.1016/j.arr.2010.09.002. Epub 2010 Sep 22.

衰老的生物学:1985-2010 年及以后。

The biology of aging: 1985-2010 and beyond.

机构信息

Departments of Pathology and Genome Sciences, University of Washington, Seattle, Washington, 98195-7470, USA.

出版信息

FASEB J. 2011 Nov;25(11):3756-62. doi: 10.1096/fj.11-1102.ufm.

DOI:10.1096/fj.11-1102.ufm
PMID:22046003
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4050331/
Abstract

In this contribution to the series of reflective essays celebrating the 25th anniversary of The FASEB Journal, our task is to assess the growth of research on the biology of aging during this period and to suggest where we might be heading during the next 25 yr. A review of the literature suggests a healthy acceleration of progress during the past decade, perhaps largely due to progress on the genetics of longevity of model organisms. Progress on the genetics of health span in these model organisms has lagged, however. Research on the genetic basis of the remarkable interspecific variations in life span has only recently begun to be seriously addressed. The spectacular advances in genomics should greatly accelerate progress. Research on environmental effects on life span and health span needs to be accelerated. Stochastic variations in gene expression in aging have only recently been addressed. These can lead to random departures from homeostasis during aging.-Martin, G. M. The biology of aging: 1985-2010 and beyond.

摘要

在这篇为庆祝《FASEB 杂志》创刊 25 周年而撰写的反思性文章系列中,我们的任务是评估在此期间衰老生物学研究的发展,并对未来 25 年的发展方向提出建议。对文献的回顾表明,过去十年的进展相当健康,这或许在很大程度上是由于模式生物的长寿遗传学方面的进展。然而,这些模式生物的健康跨度遗传学研究却滞后了。对寿命的显著种间变化的遗传基础的研究直到最近才开始得到认真解决。基因组学的惊人进展应该会大大加速这一进程。关于环境对寿命和健康跨度影响的研究需要加速。衰老过程中基因表达的随机变化最近才得到解决。这些变化会导致衰老过程中体内平衡的随机偏离。——马丁,GM 衰老的生物学:1985-2010 及以后。