Figure 1.

Acute infection of H. pylori can induce autophagy. H. pylori-OMVs stimulate NOD1, thereby triggering an autophagic response. H. pylori secretes HP0175, which upregulates UPR-dependent autophagy. VacA inhibits mTORC1, subsequently activating cellular autophagy via the ULK1 complex. VacA forms conjugates with LRP1 to regulate the formation of autophagosomes and autolysosomes. VacA can also induce autophagy via induction of ER stress. VacA can reduce GSH levels to bind LRP1 and subsequently enhance Akt phosphorylation to activate autophagy, causing CagA degradation. VacA, vacuolating cytotoxin; CagA, cytotoxin-associated gene A; LRP1, low-density lipoprotein receptor-related protein-1; ER, endoplasmic reticulum; EIF2S1, eukaryotic translation initiation factor 2 subunit 1; DDIT3, DNA damage-inducible transcript 3; ATF4, activating transcription factor 4; ULK1, Unc-51-like kinase 1; UPR, unfolded protein response; PERK, PKR-like ER kinase; PG-OMVs, peptidoglycan-outer membrane vesicles; NOD1, nucleotide-binding oligomerization domain-1; LC3, microtubule-associated protein light chain 3; GSH, glutathione; H. pylori, Helicobacter pylori; mTORC1, mTOR complex 1; VPS34, phosphatidylinositol 3-kinase catalytic subunit type 3.