Senescence is a cellular response to stress for both dividing and post-mitotic cells. Noteworthy, long-lived post-mitotic cells (collectively named LLPMCs), which can live for decades in the organism, can exhibit a distinct type of cellular aging characterized by a progressive functional decline not associated to an overt senescence phenotype. The age-related drivers of senescence and aging in LLPMCs remain largely unknown. There is evidence that an increased production of reactive oxygen species (ROS) due to dysfunctional mitochondria, coupled with an inherent inability of cellular-degradation mechanisms to remove damaged molecules, is responsible for senescence and aging in LLPMC. Although telomeric DNA shortening, by nature linked to cell division, is generally not considered as a driver of LLPMC aging and senescence, we discuss recent reports revealing the existence of age-related telomere changes in LLPMC. These findings reveal unexpected roles for telomeres in LLPMC function and invite us to consider the hypothesis of a complex telomere clock involved in both dividing and non-dividing cell aging.

衰老是分裂细胞和有丝分裂后细胞对压力的细胞反应。值得注意的是，可以在生物体中存活数十年的长寿命有丝分裂后细胞（统称为LLPMC）可以表现出独特的细胞衰老类型，其特征是进行性功能下降，与明显的衰老表型无关。LLPMC中与年龄相关的衰老和衰老驱动因素仍然未知。有证据表明，线粒体功能异常会导致活性氧（ROS）产量增加​​，再加上细胞降解机制无法清除受损分子，这是LLPMC衰老和衰老的原因。尽管本质上与细胞分裂有关的端粒DNA缩短通常不被认为是LLPMC衰老和衰老的驱动力，我们讨论了最近的报告，这些报告揭示了LLPMC中存在与年龄有关的端粒变化。这些发现揭示了端粒在LLPMC功能中的出乎意料的作用，并邀请我们考虑涉及分裂和非分裂细胞衰老的复杂端粒时钟的假说。