Is p53 a key to understanding the distinction of aging process between normal human and rodent cells?

摘要

Normal fibroblast cells have a limited capacity of cell proliferation in an in vitro cell culture model due to a process termed replicative senescence or cellular senescence . Cellular senescence has been proposed as a gatekeeping tumor sup-pressor mechanism . The tumor suppressor p53 is evolutionarily conserved across species. p53 has been implicated in many biological pro-cesses including apoptosis, cellular senescence, and cancer . A growing body of evidence sug-gests that p53 contributes to organismal aging [3-7]. It was recently reported that too much of p53 activity suppresses cancer, and shortens life span of mice . Mice carrying hyperactivated p53 exhibit signs of premature aging including osteoporosis, organ atrophy, small body size and weight, and cellular senescence .