Mair William, Dillin Andrew
The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Annu Rev Biochem. 2008;77:727-54. doi: 10.1146/annurev.biochem.77.061206.171059.
Reducing food intake to induce undernutrition but not malnutrition extends the life spans of multiple species, ranging from single-celled organisms to mammals. This increase in longevity by dietary restriction (DR) is coupled to profound beneficial effects on age-related pathology. Historically, much of the work on DR has been undertaken using rodent models, and 70 years of research has revealed much about the physiological changes DR induces. However, little is known about the genetic pathways that regulate the DR response and whether or not they are conserved between species. Elucidating these pathways may facilitate the design of targeted pharmaceutical treatments for a range of age-related pathologies. Here, we discuss how recent work in nonmammalian model organisms has revealed new insight into the genetics of DR and how the discovery of DR-specific transcription factors will advance our understanding of this phenomenon.
减少食物摄入量以诱发营养不足但非营养不良可延长从单细胞生物到哺乳动物等多种物种的寿命。通过饮食限制(DR)实现的寿命延长与对年龄相关病理的深远有益影响相关联。从历史上看,关于DR的许多研究工作都是使用啮齿动物模型进行的,70年的研究揭示了很多DR诱导的生理变化。然而,对于调节DR反应的遗传途径以及它们在物种间是否保守,我们知之甚少。阐明这些途径可能有助于设计针对一系列年龄相关病理的靶向药物治疗。在这里,我们讨论非哺乳动物模式生物的最新研究如何揭示了对DR遗传学的新见解,以及DR特异性转录因子的发现将如何推进我们对这一现象的理解。
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