SynthesisClinical and experimental medicine2025
Mechanism and role of ferroptosis in the development of gastric cancer.
Synthesis in Clinical and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- Ferroptosis and prostate cancer: A translational path from molecular mechanisms to precision therapy.Genes & diseases · 2026Review
- Review
- A clinical decision framework for redox-adapted, EMT-high cancers: From ferroptosis resistance to precision therapeutic stratification.Redox biology · 2026Review
- Phosphatidylserine Decarboxylase Promotes Ferroptosis Through STAT3/GPX4 Signaling in Gastric Cancer.Current issues in molecular biology · 2026Article
- Metallic elements and their molecular roles in gastric cancer: Pathogenic mechanisms and therapeutic implications.World journal of gastrointestinal oncology · 2026Review
- Targeting ferroptosis in osteoporosis: mechanisms and natural products therapies.Frontiers in pharmacology · 2026Review
- Harnessing the gut microbiome to modulate ferroptosis: a metabolic strategy for the treatment of digestive tract cancers.Frontiers in immunology · 2025Review
- Hypoxia-inducible factor 1-alpha: a dual regulator of ferroptosis in ischemic stroke and a promising therapeutic target.Frontiers in neurologyReview
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Gastric cancer (GC) represents a prevalent form of malignant neoplasm characterized by elevated incidence and fatality rates, limited early detection capabilities, and unfavorable clinical outcomes. Its occurrence and development involve complex biological processes. As a recently identified form of cellular demise, ferroptosis has been observed across multiple cancer types, garnering significant research interest in contemporary studies. Nevertheless, the precise regulatory networks governing ferroptosis in gastric cancer, along with its functional implications in the initiation and advancement of this malignancy, remain unclear. This study seeks to elucidate the functional significance of ferroptosis in the pathogenesis of GC, systematically review the dysregulated metabolic pathways associated with this cell death process, and elucidate the intricate interactions among ferroptosis-related signaling cascades. These investigations are expected to establish a novel conceptual framework for understanding the molecular pathogenesis of gastric cancer and identifying potential therapeutic interventions. A comprehensive literature search was conducted using PubMed to identify relevant original research articles and review papers examining the molecular mechanisms underlying ferroptosis in gastric carcinoma. The search strategy incorporated the following key terms: "Ferroptosis," "Ferroptosis and gastric cancer," "Ferroptosis and GSH," "Ferroptosis and GPX4," "Ferroptosis and system Xc-," "Iron metabolism," "lipid peroxidation," "FSP1-CoQ10," "DHODH-CoQH2," "GCH1-BH4," "ferroptosis inducer," etc. Emerging evidence from contemporary research indicates that targeted ferroptosis represents a novel and potentially efficacious treatment modality for patients with gastric cancer. Along with the identification of precise molecular targets for therapeutic intervention, the metabolic regulatory networks associated with ferroptosis remains an essential area for future research endeavors.
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