Genetic mouse models of extended lifespan

Genetic mouse models of extended lifespan
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DOI:
10.1016/j.exger.2003.10.019
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发表时间:
2003-11-01
影响因子:
3.9
通讯作者:
Richardson, A
Richardson, A
中科院分区:
医学2区
文献类型:
--
作者:
Liang, HY;Masoro, EJ;Richardson, A

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自1996年以来,已有7种遗传性小鼠模型被报道显示寿命延长:Ames和Snell侏儒小鼠,小鼠(GHRHR(LIT/LIT)),生长激素受体/结合蛋白(GHR/BP-/-)或p66(SHC-/-)缺失(p66(SHC-/-)),IGF-I受体杂合子小鼠(IgflR(+/-)),以及脂肪特异性胰岛素受体基因敲除小鼠。在这篇文章中,我们描述和评估了这些小鼠模型与衰老研究的相关性。虽然这七种遗传模型都显示出寿命的显著延长,但样本量和动物饲养程序的问题需要进一步评估,才能对大多数这些小鼠模型的寿命延长的重复性得出确切的结论。由于除了侏儒小鼠之外,所有模型都缺乏与年龄相关的病理和生理功能的数据,因此现在就得出这些小鼠模型衰老延缓的结论还为时过早。然而,这些小鼠模型已经为哺乳动物衰老的机制提供了新的信息。(C)2003 Elsevier Inc.保留所有权利。
Since 1996, seven genetic mouse models have been reported to show increased lifespan: Ames and Snell dwarf mice, the 'little mouse' (Ghrhr(lit/lit)), mice null for either growth hormone receptor/binding protein (GHR/BP-/-) or p66(shc) (p66(shc-/-)), mice heterozygous for the IGF-I receptor (Igflr(+/-)), and fat-specific insulin receptor knockout mice. In this article, we describe and evaluate these mouse models with respect to their relevance for aging studies. While these seven genetic models all show a significant increase in lifespan, issues of sample size and animal husbandry procedures require further evaluation before firm conclusions can be drawn on the reproducibility of life extension in most of these mouse models. Because data on the age-related pathology and physiological functions are lacking for all of the models, except the dwarf mice, it is too early to conclude that aging is retarded in these mouse models. However, these mouse models are already providing new information about the mechanism underlying mammalian aging. (C) 2003 Elsevier Inc. All rights reserved.