Cellular senescence is a steady cell cycle arrest that can be activated in normal cells in reaction to varied innate and extrinsic stimuli, as well as developmental indications. Senescence is deemed to be a highly vibrant, multi-step procedure, during which the properties of senescent cells constantly evolve and diversify in a context-dependent manner. It is associated with considerable cellular and molecular changes and specific phenotypic alterations, containing a stable expansion arrest unresponsive to mitogenic stimuli. Senescent cells remain viable, have alterations in metabolic activity and go through surprising modifications in gene expression and expand a complex senescence-associated secretory phenotype.

Cellular senescence can compromise tissue rehabilitation and regeneration, thereby contributing to aging. Removal of senescent cells can attenuate age-related tissue dysfunction and lengthen health span. Senescence can furthermore act as a potent anti-tumor mechanism, by deterring the proliferation of potentially cancerous cells. It is a cellular program that acts as a double-edged sword, with both beneficial and destructive impacts on the health of the organism,

Cells frequently experience anxiety and harm from exogenous and endogenous sources, and their reactions range from comprehensive comeback to cell death. Proliferating cells can begin an extra answer by adopting a condition of permanent cell-cycle arrest that is termed cellular senescence.
Understanding the causes and consequences of cellular senescence has delivered novel insights into how cells respond to stress, particularly genotoxic stress, and how this cellular reaction can impact complex organismal procedures such as the growth of cancer and aging.

Key Points
· Cellular senescence is a multifaceted procedure that apprehends the proliferation of cells that are at threat of neoplastic transformation.

· Many stimulants elicit a senescence response. These comprise dysfunctional telomeres, DNA damage, the expression of specific oncogenes, perturbations to chromatin organization, and robust mitogenic cues.

· There is now considerable evidence that cellular senescence is an obstacle to malignant tumorigenesis in vivo.

· In mammalian organisms, cells that convey markers of senescence have been shown to collect with age and at sites of specific age-related pathologies. There is furthermore mounting proof that cellular senescence contributes to aging.

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