Abstract
Cellular senescence, a permanent state of cell cycle arrest accompanied by a complex phenotype, is an essential mechanism that limits tumorigenesis and tissue damage. In physiological conditions, senescent cells can be removed by the immune system, facilitating tumor suppression and wound healing. However, as we age, senescent cells accumulate in tissues, either because an aging immune system fails to remove them, the rate of senescent cell formation is elevated, or both. If senescent cells persist in tissues, they have the potential to paradoxically promote pathological conditions. Cellular senescence is associated with an enhanced pro-survival phenotype, which most likely promotes persistence of senescent cells in vivo. This phenotype may have evolved to favor facilitation of a short-term wound healing, followed by the elimination of senescent cells by the immune system. In this review, we provide a perspective on the triggers, mechanisms and physiological as well as pathological consequences of senescent cells.
Highlights
Cellular senescence, a permanent state of cell cycle arrest accompanied by a complex phenotype, is an essential mechanism that limits tumorigenesis and tissue damage
Chromosome ends consist of a telomere end complex made up of telomeric proteins that protects chromosome ends from being recognized as a double strand break, thereby preventing a DNA damage response (DDR)
As with oncogene-induced senescence (OIS), phenotypically stress-induced premature senescence (SIPS) and replicative senescence (RS) appear to be similar in many ways, but it has been shown that they can differ at the level of protein expression [19]
Summary
Cell senescence can be induced by various stimuli, all of which engage similar molecular pathways to initiate and sustain the senescence program (Fig. 1). The first experimental evidence for the existence of such a program was provided by Hayflick and Moorehead [1] more than 50 years ago. They demonstrated that cultured cells have a maximum limit on the number of cellular divisions that can be undertaken. This replicative limit is a result of the gradual shortening of telomeres due to an inability of replicative polymerases to synthesize DNA at chromosome ends [2, 3]. An enzyme that adds telomeric repeats back to chromosome ends, protects cells from RS [5, 6]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
