Cellular senescence entails a permanent proliferative arrest, coupled to multiple phenotypic changes. Among these changes is the release of numerous biologically active molecules collectively known as the senescence-associated secretory phenotype, or SASP. A growing body of literature indicates that both senescence and the SASP are sensitive to cellular and organismal metabolic states, which in turn can drive phenotypes associated with metabolic dysfunction. Here, we review the current literature linking senescence and metabolism, with an eye toward findings at the cellular level, including both metabolic inducers of senescence and alterations in cellular metabolism associated with senescence. Additionally, we consider how interventions that target either metabolism or senescent cells might influence each other and mitigate some of the pro-aging effects of cellular senescence. We conclude that the most effective interventions will likely break a degenerative feedback cycle by which cellular senescence promotes metabolic diseases, which in turn promote senescence.

细胞衰老需要永久性增殖停滞，并伴有多种表型变化。这些变化包括大量生物活性分子的释放，这些分子统称为衰老相关分泌表型或 SASP。越来越多的文献表明，衰老和 SASP 都对细胞和有机体代谢状态敏感，这反过来又可以驱动与代谢功能障碍相关的表型。在这里，我们回顾了当前将衰老和新陈代谢联系起来的文献，着眼于细胞水平的发现，包括衰老的代谢诱导剂和与衰老相关的细胞代谢的改变。此外，我们考虑针对新陈代谢或衰老细胞的干预措施如何相互影响并减轻细胞衰老的一些促衰老作用。我们的结论是，最有效的干预措施可能会打破细胞衰老促进代谢疾病的退化反馈循环，而代谢疾病又反过来促进衰老。