Center for Molecular Medicine, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Free Radic Biol Med. 2012 Jan 15;52(2):281-90. doi: 10.1016/j.freeradbiomed.2011.10.484. Epub 2011 Oct 31.
For much of the time since their discovery, the sirtuin family of deacetylase enzymes has been associated with extension of life span. This longevity-promoting capacity in numerous model systems has enabled the sirtuins to gain "celebrity status" in the field of aging research. However, the mechanisms underpinning these changes remain incompletely defined. A general phenotype long associated with aging is the dysregulation of biological systems, which partly occurs via the accumulation of damage over time. One of the major sources of this damage is oxidative stress, which can harm both biological structures and the mechanisms with which they are repaired. It is now becoming clear that the beneficial life-span effects of sirtuins, along with many of their other functions, are closely linked to their ability to regulate systems that control the redox environment. Here we investigate the links between sirtuins and their oxidative/redox environment and review the control mechanisms that are regulated by the activity of sirtuin deacetylase proteins.
在其被发现后的大部分时间里，去乙酰化酶 sirtuin 家族一直与寿命的延长有关。在众多模型系统中，这种促进长寿的能力使 sirtuins 在衰老研究领域获得了“名人地位”。然而，这些变化背后的机制仍不完全明确。与衰老长期相关的一般表型是生物系统的失调，这部分是通过随着时间的推移积累的损伤发生的。这种损伤的主要来源之一是氧化应激，它既可以损害生物结构，也可以损害修复它们的机制。现在越来越清楚的是，sirtuins 的有益的寿命效应，以及它们的许多其他功能，与它们调节控制氧化还原环境的系统的能力密切相关。在这里，我们研究了 sirtuins 与其氧化/还原环境之间的联系，并回顾了受 sirtuin 去乙酰化酶蛋白活性调节的控制机制。
