Fig. 8.

Hypothetical model of induction and role of autophagy after membrane perforation by PFT: membrane perforation cuts nutrient supplies by paralysing ion gradient–dependent transport systems and causes energy loss. This leads to the activation of GCN2, AMPK and possibly additional pro-autophagic signals. The autophagic response triggered by these pathways can temporarily relieve energy and nutrient shortage, and might contribute to the elimination of toxin by promoting its destruction, or leading to exocytosis of undigestable pore complexes [16]