Abstract
Aging is the largest risk factor for most chronic diseases, which account for the majority of morbidity and health care expenditures in developed nations. New findings suggest that aging is a modifiable risk factor, and it may be feasible to delay age-related diseases as a group by modulating fundamental aging mechanisms. One such mechanism is cellular senescence, which can cause chronic inflammation through the senescence-associated secretory phenotype (SASP). We review the mechanisms that induce senescence and the SASP, their associations with chronic disease and frailty, therapeutic opportunities based on targeting senescent cells and the SASP, and potential paths to developing clinical interventions.
Authors
Tamara Tchkonia, Yi Zhu, Jan van Deursen, Judith Campisi, James L. Kirkland
Figure 2
A disruption of the intersection between fundamental aging mechanisms and processes that lead to chronic diseases may delay age-related diseases and disabilities as a group and thereby lengthen health span.
Copyright © 2025 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)