Fig. 1
From: Polymorphism in autophagy-related genes LRP1 and CAPZA1 may promote gastric mucosal atrophy
Putative model of autophagy as a host defense against H. pylori infection. H. pylori injects the toxic protein, CagA, into host epithelial cells. Then, CagA induces the production of pro-inflammatory cytokines. The host cell recognizes the VacA toxin secreted by H. pylori via the LRP1 receptor and induces autophagy. LRP1-ICD moves into the nucleus and increases the expression of LAMP1. Subsequently, autophagy degrades CagA. However, CAPZA1, a host protein, binds to the LRP1-ICD and inhibits LRP1-induced autophagy