ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
SENP6-Mediated deSUMOylation of Nrf2 Exacerbates Neuronal Oxidative Stress Following Cerebral Ischemia and Reperfusion Injury.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- SENP7 mediates deSUMOylation and deubiquitination of SP1 to promote lung adenocarcinoma progression and chemoresistance.Translational oncology · 2026Article
- Multiple organ dysfunction syndrome: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Biomimetic Ru-Mn Nanozyme with Cascade Catalytic Activity Attenuates Secondary Brain Injury in Intracerebral Hemorrhage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Molecularly self-assembled nanoplatforms for targeted ROS-scavenging and neuroinflammation alleviation in acute ischemic stroke.Materials today. Bio · 2026Article
- Sevoflurane ameliorates cerebral ischemia-reperfusion injury by modulating mitochondrial dynamics and attenuating apoptosis via Shh-YAP1 signaling pathway.Molecular brain · 2026Article
- SUMOylation Inhibitor TAK-981 Alleviates Hallmark Features of Preeclampsia Related to High Glucocorticoid Exposure by Inhibiting Placental Oxidative Stress in Rats.Antioxidants (Basel, Switzerland) · 2026Article
- Regulatory networks of post-translational modifications in diabetic kidney disease: from pathogenic mechanisms to therapeutic frontiers.Frontiers in endocrinology · 2026Review
- SENP6 Restrains NLRP3 Inflammasome Activation via DeSUMOylation-Driven K48-Linked Ubiquitination of NLRP3 in Acute Lung Injury.Research (Washington, D.C.) · 2026Article
- SENP3 promotes renal tubular epithelial cell apoptosis after ischemia-reperfusion injury via ASS1 deSUMOylation.Cell death & disease · 2025Article
- NIR Driven Pd/Cerium Oxide Nano-Heterojunction for Enhanced Salvaging Sepsis Induced Acute Liver Injury via Reprogramming Redox Homeostasis in Synergy with Inducing Autophagy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- SENP6-Mediated deSUMOylation of Nrf2 Exacerbates Neuronal Oxidative Stress Following Cerebral Ischemia and Reperfusion Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Post-translational modifications orchestrate mTOR-driven cell death in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
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10 authors.
Funding
Abstract
Oxidative stress is believed to play critical pathophysiological roles in ischemic brain injury, and the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway is recognized as the most crucial endogenous antioxidant stress damage route. Some research have demonstrated that Nrf2 play critical roles in oxidative stress after ischemic stroke, but the underlying mechanism are not fully elucidated. This study reveals that Nrf2 is modified by SUMOylation and identifies Sentrin/SUMO-specific protease 6 (SENP6) as a negative regulator of Nrf2 SUMOylation. Notably, SENP6 binds to and mediates the deSUMOylation of Nrf2, which in turn inhibits antioxidant response by enhancing ubiquitination-dependent degradation of Nrf2, thereby reducing its transcriptional activity, inducing oxidative stress and aggravating neuronal apoptosis after ischemic stroke. Additionally, blocking the interaction between SENP6 and Nrf2 with a cell membrane-permeable peptide (Tat-Nrf2) preserves the SUMOylation of Nrf2, effectively attenuates oxidative stress, and rescues neurological functions in mice subjected to ischemic stroke. Furthermore, no toxicity is observed when high doses Tat-Nrf2 are injected into nonischemic mice. Collectively, this study uncovers a previously unidentified mechanism whereby SUMOylation of Nrf2 regulates oxidative stress and strongly indicates that interventions targeting SENP6 or its interaction with Nrf2 may provide therapeutic benefits for ischemic stroke.
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