Aging is a global decline of physiological functions, leading to an increased susceptibility to diseases and ultimately death. Maximum lifespans differ up to 200-fold between mammalian species. Although considerable progress has been achieved in identifying conserved pathways that regulate individual lifespan within model organisms, whether the same pathways are responsible for the interspecies differences in longevity remains to be determined. Recent cross-species studies have begun to identify pathways responsible for interspecies differences in lifespan. Here, we review the evidence supporting the role of anticancer mechanisms, DNA repair machinery, insulin/insulin-like growth factor 1 signaling, and proteostasis in defining species lifespans. Understanding the mechanisms responsible for the dramatic differences in lifespan between species will have a transformative effect on developing interventions to improve human health and longevity.

中文翻译：

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决定短寿命和长寿命物种寿命的分子机制

衰老是生理功能的整体衰退，导致对疾病的易感性增加并最终导致死亡。哺乳动物物种之间的最长寿命差异高达 200 倍。尽管在确定模式生物体内调节个体寿命的保守通路方面取得了相当大的进展，但相同的通路是否是造成物种间寿命差异的原因仍有待确定。最近的跨物种研究已经开始确定导致物种间寿命差异的途径。在这里，我们回顾了支持抗癌机制、DNA 修复机制、胰岛素/胰岛素样生长因子 1 信号传导和蛋白质稳态在定义物种寿命中的作用的证据。