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Cellular senescence has been defined as an irreversible cell cycle arrest which stops the propagation of damaged cells. It was very first observed by Hayflick and Moorhead who demonstrated a limited replicative lifespan of human fibroblasts in culture (Hayflick Moorhead, 1961). A number of stressors such as the shortening of telomeres, DNA lesions, oncogene activation, oxidative anxiety and others can induce cellular senescence (van Deursen, 2014). Based on the trigger, senescence may be executed by numerous diverse effector pathways. The key ones comprise the p53-p21 and p16 pathways. Senescent cells knowledge dramatic changes at the degree of gene expression, mitochondrial function (Correia-Melo et al., 2016) and epigenome (Cruickshanks et al., 2013). In addition, senescent cells have already been shown to have a distinct secretome profile, known as senescence-associated secretory phenotype (SASP) (Copp et al., 2008). SASP involves development elements, extracellular e matrix degrading proteins and pro-inf.
