![]() ![]() Activation of the p53/p21 WAF1/CIP1 and p16 INK4A/pRB tumor suppressor pathways play a central role in regulating senescence. ![]() 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. Senescence can also act as a potent anti-tumor mechanism, by preventing proliferation of potentially cancerous cells. Removal of senescent cells can attenuate age-related tissue dysfunction and extend health span. Cellular senescence can compromise tissue repair and regeneration, thereby contributing toward aging. ![]() Senescent cells remain viable, have alterations in metabolic activity and undergo dramatic changes in gene expression and develop a complex senescence-associated secretory phenotype. It is associated with multiple cellular and molecular changes and distinct phenotypic alterations, including a stable proliferation arrest unresponsive to mitogenic stimuli. 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. MRC Prion Unit at UCL, UCL Institute of Prion Diseases, London, United KingdomĬellular 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.
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