Cellular senescence is a stable cell cycle arrest that can be triggered in 
normal cells in response to various intrinsic and extrinsic stimuli, as well as 
developmental signals. Senescence is considered to be a highly dynamic, 
multi-step process, during which the properties of senescent cells continuously 
evolve and diversify in a context dependent manner. It is associated with 
multiple cellular and molecular changes and distinct phenotypic alterations, 
including a stable proliferation arrest unresponsive to mitogenic stimuli. 
Senescent cells remain viable, have alterations in metabolic activity and 
undergo dramatic changes in gene expression and develop a complex 
senescence-associated secretory phenotype. Cellular senescence can compromise 
tissue repair and regeneration, thereby contributing toward aging. Removal of 
senescent cells can attenuate age-related tissue dysfunction and extend health 
span. Senescence can also act as a potent anti-tumor mechanism, by preventing 
proliferation of potentially cancerous cells. It is a cellular program which 
acts as a double-edged sword, with both beneficial and detrimental effects on 
the health of the organism, and considered to be an example of evolutionary 
antagonistic pleiotropy. Activation of the p53/p21WAF1/CIP1 and p16INK4A/pRB 
tumor suppressor pathways play a central role in regulating senescence. Several 
other pathways have recently been implicated in mediating senescence and the 
senescent phenotype. Herein we review the molecular mechanisms that underlie 
cellular senescence and the senescence associated growth arrest with a 
particular focus on why cells stop dividing, the stability of the growth arrest, 
the hypersecretory phenotype and how the different pathways are all integrated.