(Left) Under normal conditions, autophagy alleviates stressors that can cause cellular senescence such as dysfunctional mitochondria, ROS, and ER stress. Autophagy also maintains the lysosomal integrity, thus acting an anti-senescence mechanism in a passive manner. p62-dependent autophagy, meanwhile, specifically degrades GATA4, a main regulator of the SASP, thereby actively suppressing cellular senescence. (Right) Autophagy function as ‘non-senescence addiction’ that can manage several senescence-associated stresses and thus maintain the viability of senescent cells. In addition, autophagy targets Δ133p53α or lamin B to cause cellular senescence. Lastly, autophagy may provide amino acids to support the massive synthesis of some SASP factors through the TASCC.