Targeting ferroptosis in Helicobacter pylori-associated gastric cancer development: From molecular mechanisms to application prospects (Review)

Abstract

Gastric cancer (GC) has a high incidence, resistance to chemotherapeutic drugs and a bleak prognosis. Helicobacter pylori (H. pylori) can promote GC development through Correa's cascade by impacting various forms of programmed cell death (PCD). As an iron-dependent form of PCD, ferroptosis has emerged as a major focus in biomedical research. Notably, there have been developments in elucidating the mechanisms underlying ferroptosis dysregulation throughout Correa's cascade. On one hand, targeting ferroptosis may provide a promising direction for the development of drugs for chronic atrophic gastritis (CAG) and intestinal metaplasia (IM). On the other hand, targeting ferroptosis in GC may be a potential option to overcome the challenges in conventional therapies such as resistance to chemotherapy. Consequently, the present review aims to deliver a comprehensive understanding of the mechanisms underlying ferroptosis dysregulation in H. pylori-associated GC and summarize the latest progress of ferroptosis-related studies in CAG, IM and GC. The present study identifies key regulators of ferroptosis at distinct pathological stages, thereby providing insight of novel strategies for the management of precancerous lesion-related diseases and GC.