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Fig. 1. Dual roles of autophagy in the regulation of cellular senescence.

(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.

Mol. Cells 2017;40:607~612
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