Role of sirtuins, calorie restriction and physical activity in aging.

Role of sirtuins, calorie restriction and physical activity in aging.
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DOI:
10.2741/e417
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发表时间:
2012
期刊:
Frontiers in bioscience
影响因子:
--
通讯作者:
G. Corbi;V. Conti;G. Scapagnini;A. Filippelli;N. Ferrara
G. Corbi;V. Conti;G. Scapagnini;A. Filippelli;N. Ferrara
中科院分区:
其他
文献类型:
--
作者:
G. Corbi;V. Conti;G. Scapagnini;A. Filippelli;N. Ferrara

文献摘要

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最近发现Sirtuins代表寿命的关键调节因子。热量限制(CR)可以延长从酵母到哺乳动物的寿命。虽然Sirt-1和CR之间的关系是明确的,但Sir 2增加寿命的分子机制仍然未知。在哺乳动物中,CR诱导生理和行为变化,许多研究表明,CR减少活性氧的产生,从而最大限度地减少氧化损伤,导致CR通过减少氧化应激延长寿命的假设。事实上,衰老和年龄相关疾病的病理生理学涉及氧化应激作为其发展的早期阶段。最近我们发现,在老年大鼠中,心脏和脂肪组织中的SIRT 1活性降低,这表明衰老在体内的特征是这种长寿关键调节因子的效率降低。虽然有几项研究报告说,增加体力活动可以通过降低许多与年龄有关的疾病的死亡风险来提高平均寿命,但运动和长寿研究未能证明运动对最长寿命的影响。然而,在老年大鼠中,适度的长时间运动训练能够诱导SIRT 1活性的增加,这表明该工具可以抵消与年龄相关的功能障碍。
Recently it has been discovered that Sirtuins represent pivotal regulators of lifespan. Caloric restriction (CR) enhances longevity from yeast to mammals. Whereas the relationship between Sirt-1 and CR is clear, the molecular mechanisms by which Sir2 increases longevity are still unknown. In mammals, CR induces physiological and behavioral changes, and many studies have shown that CR decreases production of reactive oxygen species production thus minimizing oxidative damage, leading to the hypothesis that CR by reducing oxidative stress extends the lifespan by counteraction of aging. In fact, the pathophysiology of aging and age-related diseases involves oxidative stress as an early stage in its development. Recently we found that in aged rats the SIRT1 activity was decreased in heart and adipose tissue, showing as aging is characterized in vivo by a reduced efficiency of this key-regulator of longevity. Whereas several studies have reported that increased physical activity can improve mean life span presumably by reducing mortality risk from many age-related diseases, exercise and longevity studies have failed to document an exercise effect on maximum life span. However, in aged rats a moderate prolonged exercise training is able to induce increase in SIRT1 activity, suggesting that this tool could counteract age-related dysfunctions.