Suppr超能文献

由不同机制导致的加速衰老小鼠的比较。

Comparison of mice with accelerated aging caused by distinct mechanisms.

作者信息

Gurkar Aditi U, Niedernhofer Laura J

机构信息

Department of Metabolism and Aging, Scripps Florida, 130 Scripps Way #3B3, Jupiter, FL 33458, USA.

Department of Metabolism and Aging, Scripps Florida, 130 Scripps Way #3B3, Jupiter, FL 33458, USA.

出版信息

Exp Gerontol. 2015 Aug;68:43-50. doi: 10.1016/j.exger.2015.01.045. Epub 2015 Jan 21.

Abstract

Aging is the primary risk factor for numerous chronic, debilitating diseases. These diseases impact quality of life of the elderly and consume a large portion of health care costs. The cost of age-related diseases will only increase as the world's population continues to live longer. Thus it would be advantageous to consider aging itself as a therapeutic target, potentially stemming multiple age-related diseases simultaneously. While logical, this is extremely challenging as the molecular mechanisms that drive aging are still unknown. Furthermore, clinical trials to treat aging are impractical. Even in preclinical models, testing interventions to extend healthspan in old age are lengthy and therefore costly. One approach to expedite aging studies is to take advantage of mouse strains that are engineered to age rapidly. These strains are genetically and phenotypically quite diverse. This review aims to offer a comparison of several of these strains to highlight their relative strengths and weaknesses as models of mammalian and more specifically human aging. Additionally, careful identification of commonalities among the strains may lead to the identification of fundamental pathways of aging.

摘要

衰老乃是众多慢性、使人衰弱疾病的主要风险因素。这些疾病影响老年人的生活质量,并耗费了大部分医疗保健费用。随着世界人口寿命的持续延长,与年龄相关疾病的成本只会增加。因此,将衰老本身视为一个治疗靶点,有可能同时遏制多种与年龄相关的疾病,这将是有益的。虽然这合乎逻辑,但极具挑战性,因为驱动衰老的分子机制仍然未知。此外,针对衰老进行治疗的临床试验并不切实可行。即便在临床前模型中,测试延长老年健康寿命的干预措施也耗时漫长,因而成本高昂。加速衰老研究的一种方法是利用经过基因工程改造而快速衰老的小鼠品系。这些品系在基因和表型上差异很大。本综述旨在对其中几种品系进行比较,以突出它们作为哺乳动物尤其是人类衰老模型的相对优势和劣势。此外,仔细识别品系之间的共性可能会促成对衰老基本途径的识别。

相似文献

1
Comparison of mice with accelerated aging caused by distinct mechanisms.由不同机制导致的加速衰老小鼠的比较。
Exp Gerontol. 2015 Aug;68:43-50. doi: 10.1016/j.exger.2015.01.045. Epub 2015 Jan 21.
3
Aging. Genomic priorities in aging.衰老。衰老过程中的基因组优先事项。
Science. 2002 May 17;296(5571):1250-1. doi: 10.1126/science.1071808. Epub 2002 Apr 11.
5
Premature aging in mice deficient in DNA repair and transcription.DNA修复和转录缺陷小鼠的早衰
Science. 2002 May 17;296(5571):1276-9. doi: 10.1126/science.1070174. Epub 2002 Apr 11.
6
O-GlcNAc modification affects the ATM-mediated DNA damage response.O-连接的N-乙酰葡糖胺修饰影响ATM介导的DNA损伤反应。
Biochim Biophys Acta. 2012 Oct;1820(10):1678-85. doi: 10.1016/j.bbagen.2012.06.013. Epub 2012 Jul 1.
8
ATM and ATR.共济失调毛细血管扩张症突变基因(ATM)和Rad3相关蛋白(ATR)
Curr Biol. 2003 Jun 17;13(12):R468. doi: 10.1016/s0960-9822(03)00403-2.

引用本文的文献

1
9
Skeletal phenotypes and molecular mechanisms in aging mice.衰老小鼠的骨骼表型和分子机制。
Zool Res. 2024 Jul 18;45(4):724-746. doi: 10.24272/j.issn.2095-8137.2023.397.
10
Rodent models of AKI and AKI-CKD transition: an update in 2024.2024 年急性肾损伤和 AKI 向 CKD 进展的啮齿动物模型研究进展
Am J Physiol Renal Physiol. 2024 Apr 1;326(4):F563-F583. doi: 10.1152/ajprenal.00402.2023. Epub 2024 Feb 1.

本文引用的文献

2
Policy: NIH plans to enhance reproducibility.政策:NIH 计划提高可重复性。
Nature. 2014 Jan 30;505(7485):612-3. doi: 10.1038/505612a.
7
Nucleotide excision repair in eukaryotes.真核生物中的核苷酸切除修复。
Cold Spring Harb Perspect Biol. 2013 Oct 1;5(10):a012609. doi: 10.1101/cshperspect.a012609.
10
Photoaging.光老化
J Invest Dermatol. 2013 Jul 1;133(E1):E2-6. doi: 10.1038/skinbio.2013.176.

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