Based on bioinformatics, SESN2 negatively regulates ferroptosis induced by ischemia reperfusion via the System Xc-/GPX4 pathway
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View abstract on PubMed
Summary
This summary is machine-generated.Cerebral ischemia-reperfusion (IR) injury involves ferroptosis in brain microvascular endothelial cells. The study identifies SESN2 as a key regulator that alleviates ferroptosis via the System Xc-/GPX4 pathway, offering a potential therapeutic target.
Area Of Science
- Neuroscience
- Cell Biology
- Biochemistry
Background
- Cerebral ischemia-reperfusion (IR) injury is a significant cause of secondary brain damage.
- Ferroptosis has been implicated in IR-induced brain injury, but its role in brain microvascular endothelial cells (BMVECs) remains unclear.
Purpose Of The Study
- To investigate the role of ferroptosis in IR-induced BMVECs injury.
- To identify key regulatory genes involved in this process.
Main Methods
- Oxygen-glucose deprivation/reoxygenation (OGDR) in bEND.3 cells and a focal cerebral IR model in mice were used.
- Transcriptomic sequencing and bioinformatics analyses (Venn, PPI, MCODE) were performed.
- Mechanistic studies involving SESN2 silencing and overexpression were conducted.
Main Results
- Nine ferroptosis-related differentially expressed genes (DEGs) and six hub genes were identified.
- IR induced elevated ferroptosis indicators and decreased expression of System Xc- and GPX4.
- SESN2 was identified as a key antioxidant regulator and a negative regulator of ferroptosis.
Conclusions
- Ferroptosis plays a critical role in IR-induced BMVECs injury.
- SESN2 acts as a negative regulator of ferroptosis by activating the System Xc-/GPX4 pathway.
- Enhancing SESN2 expression may offer a therapeutic strategy to mitigate IR-induced brain injury.
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