Table 1 Virulence factors of H. pylori-associated with ferroptosis.

From: Infection of Helicobacter pylori contributes to the progression of gastric cancer through ferroptosis

Virulence factors

Effect

Reference

CagA

promotes the synthesis of PUFA-ePLs

[49]

NOX4/NRF2/GPX4 pathway mediates CagA

[20]

increases iron uptake through transferrin endocytosis and decreases cytoplasmic labile iron pool while increasing lysosomal iron

[50]

iron deficiency could enhance the virulence of H. pylori

[50]

VacA

elevates ROS levels

[55,56,57]

impairs GSH metabolism

[58, 59]

Nap

Nap binds Fe2+ ions, which are further oxidized to Fe3+

[61, 62, 67]

SodB

FecA1 is an essential gene for SodB activation

[69]

Fur is a direct regulator of SodB

[71]

gGT

catabolize reduced GSH into glutamate and cysteinylglycine (Cys-Gly)

[72]

LPS

increased GPX4 expression and elevated ROS production

[73]

OipA

decreased Xc− expression

[74]

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