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The process of cellular senescence was first described in a seminal study by Hayflick and Moorhead (1961) in which they observed that normal human fibroblasts were able to enter a state of irreversible growth arrest after serial cultivation in vitro; meanwhile cancer cells did not enter this growth arrest state and proliferated indefinitely. Hayflick and Moorhead (1961) presciently hypothesized the existence of cellular factors, whose loss through consecutive cell divisions limited the proliferation of normal cells. They went on to speculate that this “stopwatch” could be behind the process of organismal aging.

 

Today, cellular senescence is considered a stress response triggered by a number of “counting mechanisms,” such as telomere shortening, that are increasingly well understood at the molecular level. Importantly, the mechanisms underlying cellular senescence are involved in protection against cancer and also may be involved in organismal aging. It is important to emphasize here that although senescent cells in vitro may remain viable essentially indefinitely—albeit incapable of proliferation—the situation in vivo may be more complex.

 

cellThere are examples of in vivo senescent cells that may reside for years in the organism, such as the senescent melanocytes of moles or nevi (Michaloglou et al., 2005), and there are also examples of senescent cells that are rapidly removed by phagocytic cells, as in the case of senescent tumor cells in liver carcinomas (Xue et al., 2007). In the case of physiological aging, the increase in senescent cells is measurable but modest (Dimri et al., 1995).
 
However, senescence may contribute to aging not only by net accumulation of senescent cells in tissues, but also by limiting the regenerative potential of stem cell pools. These two mechanisms—namely, accumulation of senescent cells and loss of stem cell function—probably contribute to aging simultaneously.

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