ArticleFrontiers in genetics2024
Based on bioinformatics, SESN2 negatively regulates ferroptosis induced by ischemia reperfusion via the System Xc-/GPX4 pathway.
Article in Frontiers in genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Review
- Insights into the potential pathogenesis and therapeutic implications of ferroptosis in brain microvascular endothelial cells during stroke.Frontiers in immunology · 2026Review
- Ginsenoside Rg1 antagonizes diabetic osteoporosis by regulating ferroptosis via mitochondrial membrane potential in H-type vascular endothelial cells.Frontiers in aging · 2026Article
- Ferroptosis in neurodegenerative diseases: potential mechanisms of exercise intervention.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
9 authors.
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Abstract
Introduction: Cerebral ischemia-reperfusion (IR) causes severe secondary brain injury. Previous studies have demonstrated that ferroptosis is involved in IR-induced brain injury. However, whether IR induces ferroptosis in brain microvascular endothelial cells (BMVECs) is not fully understood. Materials and methods: Oxygen-glucose deprivation/reoxygenation (OGDR) was performed in bEND.3 cells to mimic IR injury Results: Using Venn analysis, nine ferroptosis-related DEGs were identified, namely, Discussion: These results suggest that SESN2 is a negative regulator of ferroptosis. Enhancing the expression of SESN2 can alleviate ferroptosis through the activation of the System Xc-/GPX4 pathway. By integrating bioinformatics analysis with mechanistic exploration, this study revealed that ferroptosis plays a crucial role in IR-induced BMVECs injury, with SESN2 acting as a negative regulator via the System Xc-/GPX4 pathway.
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