Telomere shortening accompanies mammalian aging in vivo, and the burden of senescent cells with short telomeres and a senescence-associated secretory phenotype (SASP) increases with aging. The release into the cytoplasm and the extracellular vesicle-mediated intercellular exchange of telomeric TTAGGG repeats could exert an anti-inflammatory activity by preventing the activation of the misplaced nucleic acid-sensing pathway. Many pharmacological and genetic strategies have been developed to prevent telomere shortening or to achieve telomere elongation. Recently, it was demonstrated that telomere elongation can be obtained – without genetic manipulation – by culturing mice embryonic stem cells into appropriate media. Based on this observation, we hypothesize that environmental factors could affect the initial length of telomeres by modulating the activity of telomerase during the early stages of pregnancy. Therefore, organisms with longer telomeres could exploit the anti-inflammatory activity of telomeric sequences over an extended time span, eventually delaying the development and progression of age-related diseases.

端粒缩短伴随哺乳动物体内衰老，端粒短和衰老相关的分泌表型（SASP）的衰老细胞的负担会随着年龄的增长而增加。端粒TTAGGG重复序列释放到细胞质中和胞外囊泡介导的细胞间交换可通过阻止错位的核酸传感途径的激活而发挥抗炎活性。已经开发出许多药理和遗传学策略来防止端粒缩短或实现端粒延长。最近，有研究表明，通过将小鼠胚胎干细胞培养到适当的培养基中，无需进行基因操作即可获得端粒延长。基于这一观察，我们假设环境因素可能会通过在妊娠早期调节端粒酶的活性来影响端粒的初始长度。因此，具有较长端粒的生物可以在延长的时间跨度内利用端粒序列的抗炎活性，最终延迟与年龄有关的疾病的发展和进程。