New Targets for the Identification of an Anti-Inflammatory Anti-Senescence Activity

Abstract

Aging is necessarily associated to cell senescence, but is it its sole motor or phenomenon? Replicative cell senescence can be accelerated by stress, inflammation and uneven life conditions. We talk about stress-induced premature senescence when cell metabolism is exposed to a systemic profile of cortisol and catecholamines and inflammation is maintained by a high profile of cytokines. These latter are detrimental for cells and stem-cells, accelerating the senescence of both.