ArticleCell death & disease2024
GPx1 deficiency confers increased susceptibility to ferroptosis in macrophages from individuals with active Crohn's disease.
Article in Cell death & disease, 2024. 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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Who cites it
8 citing papers in PubMed.
- Metabolic Mechanisms of Hexavalent Chromium-Induced Splenic Immune Injury via Oxidative Stress and Ferroptosis Pathways in New Zealand Rabbits.Metabolites · 2026Article
- Integrated molecular, microRNA, and biochemical profiling reveals oxidative stress-driven degeneration of the ligamentum flavum in lumbar spinal stenosis.Scientific reports · 2026Article
- 8-Epi-Prostaglandin F2α as a Redox Biomarker in Inflammatory Bowel Disease.Biomedicines · 2026Article
- A Zeolitic Pyrimidine Framework (ZPF) Nanoplatform Co-Delivers a DNAzyme and a Protein Prodrug for Cascade-Activated Tumour Therapy.Cell proliferation · 2026Article
- Spatiotemporal dynamics of reactive oxygen species: implications for cellular homeostasis and redox therapies.Cellular & molecular biology letters · 2026Review
- Sodium Butyrate Alleviates IBD by Modulating SIRT1-Involved Ferroptosis and Inhibition of Macrophage Ferroptosis.Nutrients · 2026Article
- Exploring the impact of DEP on pediatric Crohn's disease using machine learning and molecular docking methods.Frontiers in pediatrics · 2026Article
- Macrophage dysregulation in inflammatory bowel disease: cellular heterogeneity, pathogenic mechanism, and treatment.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
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Abstract
Intestinal cell death is a defining feature of Crohn's disease (CD), a major form of inflammatory bowel disease. The focus on this aspect of enteric inflammation has mainly been on epithelial cells, while other cell types such as stromal and myeloid cells have received less attention. Hypothesising that decreased macrophage viability in an oxidative environment could be a contributing factor to the pathophysiology of CD, we found that monocyte-derived macrophages from individuals with active CD (but not those in clinical disease remission) have increased sensitivity to cell death induced by H
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