The uncoupling of senescence phenotype and the inflammatory component of SASP (senescent-associated secretory phenotype) was discovered in long‐lived blind mole rat, Spalax, adapted to extreme environments. Cellular senescence in Spalax, evidenced by increased SA‐β‐Gal activity, upregulation of p21/p16/p53, is not accompanied by accumulation of DNA damage nor by secretion of SASP factors. We suggest that genome integrity, inhibition of NF‐κB nuclear translocation, and IL1α suppression are involved in overcoming the inflammatory response in aging Spalax.
We propose that suppression of SASP in senescent Spalax cells, as well as inhibition of inflammation in aging Spalax, can support a nonpermissive microenvironment for cancer progression, as well as the suppression of sterile inflammation, which is the cause of most aging‐related pathologies