Editorial Volume 12, Issue 16 pp 15875—15877

Figure 1. Schematic diagram showing the differences between canonical inflammatory SASP (human / mouse) and non-inflammatory secretome (NIS) in Spalax and their effects on homeostasis in aging tissues. Canonical secretome of senescent cells comprises a specific pattern of inflammatory mediators and growth factors that may induce senescence in surrounding cells, an effect known as "bystander senescence". The accumulation of senescent cells in aging leads to the amplification of SASP, which in turn modulates the surrounding tissues and causes the so-called "sterile inflammation"- a microenvironment that supports most age-related pathologies, including malignant neoplasms. Due to the efficient DNA repair and other mechanisms, Spalax senescent cells do not produce the main inflammatory factors that are involved in the development of age-related pathologies. Hence, when these cells transmit senescence to surrounding cells via the paracrine factors of "non-inflammatory secretome" (NIS), the recipient cells also do not elicit an inflammatory response and therefore cannot maintain "sterile inflammation" and cancer development in older Spalax.