Senescence is a process related to the stopping of divisions and changes leading the cell to the SASP phenotype. Permanent senescence of many SASP cells contributes to faster aging of the body and development of age-related diseases due to the release of pro-inflammatory factors. Both mitotically active and non-dividing cells can undergo senescence as a result of activation of different molecular pathways. Telomeres, referred to as the molecular clock, direct the dividing cell into the aging pathway when reaching a critical length. In turn, the senescence of postmitotic cells depends not on the length of telomeres, but their functionality. Dysfunctional telomeres are responsible for triggering the signaling of DNA damage response (DDR). Telomerase subunits in post-mitotic cells translocate between the nucleus, cytoplasm and mitochondria, participating in the regulation of their activity. Among other things, they contribute to the reduction of reactive oxygen species generation, which leads to telomere dysfunction and, consequently, senescence. Some proteins of the shelterin complex also play a protective role by inhibiting senescence-initiating kinases and limiting ROS production by mitochondria.

衰老是与分裂和改变的停止有关的过程，其导致细胞达到SASP表型。由于释放促炎因子，许多SASP细胞的永久衰老​​有助于身体更快的衰老和与年龄有关的疾病的发展。由于不同分子途径的激活，有丝分裂活跃的细胞和非分裂的细胞均可经历衰老。当达到临界长度时，端粒被称为分子钟，它将分裂细胞引导到衰老途径。反过来，有丝分裂后细胞的衰老并不取决于端粒的长度，而取决于它们的功能。功能失调的端粒负责触发DNA损伤反应（DDR）的信号传导。有丝分裂后细胞中的端粒酶亚基易位于细胞核，细胞质和线粒体之间，参与其活动的调节。其中，它们有助于减少活性氧的产生，从而导致端粒功能障碍，进而导致衰老。防护素复合物的某些蛋白质还通过抑制衰老引发的激酶和限制线粒体产生ROS发挥保护作用。