Figure 3.

Cellular senescence (i.e., permanent cessation of cell division) is triggered by a variety of stresses. The tumor suppressor p16 ^INK4, as well as the p53 and p21 proteins, function as cyclin-dependent kinase inhibitors, preventing phosphorylation of the Rb protein and consequently arresting the cell cycle. They release SASP factors which severely damage neighboring cells. Senescent cells can escape apoptosis by upregulation of pro-survival pathways (SCAPs = senescent cell antiapoptotic pathways). Senolytic therapies primarily target SCAPs, as exemplified in Table 1.