|Title||Rapamycin and the inhibition of the secretory phenotype.|
|Publication Type||Journal Article|
|Year of Publication||2017|
|Authors||Wang R, Sunchu B, Perez VI|
|Date Published||2017 08|
|Keywords||Animals, Cell Cycle Checkpoints, Cellular Senescence, Fibroblasts, Humans, NF-E2-Related Factor 2, Phenotype, Protein Kinase Inhibitors, Signal Transduction, Sirolimus, TOR Serine-Threonine Kinases|
Senescent cells contribute to age-related pathology and loss of function, and their selective removal improves physiological function and extends longevity. Cell senescence is a complex process that can be triggered by multiple challenges. Recently it has been observed that the composition of the secretory phenotype or SASP depends on the insult that triggers cell senescence. Rapamycin, an inhibitor of mTOR that increases longevity in several species, inhibits cell senescence in vitro, while silencing the Nrf2 gene induces premature senescence. We have found that rapamycin activates the Nrf2 pathway to regulate cell cycle arrest, but not the production of SASP, which is regulated by a different pathway, probably involving the inhibition of MAPKAPK2.
|Alternate Journal||Exp. Gerontol.|