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Moreover, senescent immune cells of various organs release pro-inflammatory cytokines (for example tumor necrosis factor (TNF-), interleukin 1 (IL-1) and IL-6), chemokines or matrix metalloproteinases, which contribute to the development of a rather pro-inflammatory phenotype, the so-called senescence-associated secretory phenotype (SASP), causing DNA damage and a state of chronic systemic lowgrade inflammation [8, 16, 25,26,27,28,29]