Table 1. Evidence for the involvement of Akt and Stat3 in cellular senescence.
Cells | Type of CS | Changes in activity/expression | Reference |
IMR90 human lung fibroblasts | Replicative CS H2O2-induced CS | Increased Akt-1 and p-Akt-1 levels in senescent cells | [48] |
Human vascular smooth muscle cells (VSMCs) | Replicative CS | Increased p-Akt level in senescent cells | [49] |
EJ p53-null human bladder cancer cells | Replicative CS p53-induced CS | Increased p-Akt (pS473 and pT308) protein level in senescent cells | [46] |
TIG3 human fibroblasts | Replicative CS IL-6-induced or soluble IL-6Rα- induced CS |
Stat3 was constitutively activated in senescent cells (both with or without exogenous IL-6/ IL-6Rα stimulation) | [50] |
Human umbilical vein endothelial cells (HUVECs) | TNFα-induced CS | Increased p-Stat1 and p-Stat3 levels in senescent cells | [51] |
IPF-derived lung fibroblasts | Replicative CS | Hyperphosphorylation of Stat3 in IPF-derived lung fibroblasts with features of CS | [52] |