Normal cells have a finite replicative life span when cultured in vitro due to a process termed replicative senescence (RS) or a much broader term cellular senescence (CS). RS is an intrinsic property that normal cells (mitotic) reach after completely exhausting their proliferative poten-tial. There has been an open debate whether rep-licative senescence contributes to organismal aging. Initial idea that replicative senescence may explain organismal aging stemmed from three lines of evidence that are correlated (e.g., donor age versus remaining replicative potential (RRP), species life span versus RRP, and cells from pre-mature aging progeroid syndrome patients versus RRP).
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