Main findings: Spalax fibroblasts undergo replicative senescence and etoposide‐induced senescence, evidenced by an increased activity of SA‐β‐Gal, growth arrest, and increased p21, p16, and p53 (Fig. A);
Yet, unlike mouse and human fibroblasts, Spalax senescent cells showed undetectable or decreased expression of the well‐known SASP factors (Fig. B);
High efficiency of DNA repair is responsible to suppression of inflammatory response in Spalax (Fig C);
Downregulation of SASP secretion in Spalax senescent fibroblasts is associated, at list in part with suppression of IL1α cytokine response and inhibition of NF-kB translocation to the nuclei (Figs. D and E); Evaluation of SASP in ageing Spalax tissues confirmed downregulation of inflammatory‐related genes (Fig. F)