Cellular senescence
Cellular senescence is the phenomenon by which normal diploid cells cease to divide. In culture, fibroblasts can reach a maximum of 50 cell divisions before becoming senescent. This phenomenon is known as "replicative senescence", or the Hayflick limit. Replicative senescence is the result of telomere shortening that ultimately triggers a DNA damage response. Cells can also be induced to senesce via DNA damage in response to elevated reactive oxygen species (ROS), activation of oncogenes and cell-cell fusion, independent of telomere length. As such, cellular senescence represents a change in "cell state" rather than a cell becoming "aged" as the name confusingly suggests. Nonetheless, the number of senescent cells in tissues rises substantially during normal aging.
Although senescent cells can no longer replicate, they remain metabolically active and commonly adopt an immunogenic phenotype consisting of a pro-inflammatory secretome, the up-regulation of immune ligands, a pro-survival response, promiscuous gene expression (pGE) and stain positive for senescence-associated β-galactosidase activity. Senescence-associated beta-galactosidase, along with p16Ink4A, is regarded to be a biomarker of cellular senescence. Nonetheless, false positives exist for maturing tissue macrophages and senescence-associated beta-galactosidase as well as for T-cells p16Ink4A.
A Senescence Associated Secretory Phenotype (SASP) consisting of inflammatory cytokines, growth factors, and proteases is another highly characteristic feature of senescent cells. SASP contributes to many age-related diseases, including type 2 diabetes and atherosclerosis. The damaging effects of SASP have motivated researchers to develop senolytic chemicals that would kill and eliminate senescent cells to improve health in the elderly. Healthy mice treated with senolytics have shown improved cardiac and vascular, function. Removal of senescent cells in normal mice increased healthspan as well as life expectancy,
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