Mitochondrial dysfunction and stem cell exhaustion are among the nine separate hallmarks of aging. Emerging evidence however suggests that mitochondrial activity can have a profound influence on the self-renewal and function of stem cells, thus mechanistically linking mitochondrial function and stem cell decline. In this review, we discuss how accumulation of mtDNA mutations or alterations in mitochondrial dynamics, turnover, and signaling can modulate age-dependent stem cell function. Finally, we also describe how mitochondrial substrate utilization influences stem and progenitor activity. Together, this growing body of evidence suggests that modulation of mitochondrial activity might provide a strategy to slow or reverse age-dependent stem cell decline, and potentially, slow or reverse human aging.

线粒体功能障碍和干细胞耗竭是衰老的九个独立标志之一。然而，新出现的证据表明，线粒体活动可以对干细胞的自我更新和功能产生深远的影响，从而在机制上将线粒体功能和干细胞衰退联系起来。在这篇综述中，我们讨论了 mtDNA 突变的积累或线粒体动力学、周转和信号传导的改变如何调节年龄依赖性干细胞功能。最后，我们还描述了线粒体底物利用如何影响茎和祖细胞的活性。总之，越来越多的证据表明，线粒体活动的调节可能提供一种减缓或逆转年龄依赖性干细胞衰退的策略，并可能减缓或逆转人类衰老。