More than 50 years ago, Hayflick et al. found that no long-lived, proliferative cells remained in long-term cell culture experiments; this phenomenon is called "cellular senescence." This finding has allowed us to understand basic individual tissue aging and cancer inhibition from the view of cellular aging. Senescent cells survive and accumulate in the body, and secrete various inflammatory cytokines or chemokines, which is different from the cell fate in apoptosis. These phenomena describe the so-called senescence-associated secretory phenotype, and chronic inflammation and carcinogenesis are induced in the surrounding tissue through senescence-associated secretory phenotype factors. For example, senescence-associated T cells are an age-dependent CD4(+ ) T-cell subpopulation with a PD-1(+ ) memory phenotype; these cells do not proliferate in response to T-cell receptor stimulation, and produce abundant osteopontin, as well as inflammatory cytokines. Senescence-associated T cells are also increased in adipose tissue under a high-fat diet, which might be related to the progress of obesity or diabetes. These series of findings might allow us to connect senescent cells and tissue aging, leading to individual aging. Interestingly, the depletion of senescent cells in the body, called senolysis, successfully increases lifespan and attenuates age-related diseases. This novel therapy is now moving forward to translational research from the bench toward clinical trials. Geriatr Gerontol Int 2020; 20: 97-100.
Keywords: biology; senescence; serology/immunology.
© 2019 Japan Geriatrics Society.