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Cellular senescence has been defined as an irreversible cell cycle arrest which stops the propagation of broken cells. It was initially observed by Hayflick and Moorhead who demonstrated a limited replicative lifespan of human fibroblasts in culture (Hayflick Moorhead, 1961). A number of stressors for instance the shortening of telomeres, DNA lesions, oncogene activation, oxidative pressure and other people can induce cellular senescence (van Deursen, 2014). Based on the trigger, senescence is usually executed by several distinctive effector pathways. The main ones comprise the p53-p21 and p16 pathways. Senescent cells encounter dramatic modifications at the degree of gene expression, mitochondrial function (Correia-Melo et al., 2016) and epigenome (Cruickshanks et al., 2013). Furthermore, senescent cells have been shown to have a distinct secretome profile, called senescence-associated secretory phenotype (SASP) (Copp et al., 2008). SASP consists of growth variables, extracellular e matrix degrading proteins and pro-inf.
