ArticleJournal of cellular and molecular medicine2024
SENP1 reduces oxidative stress and apoptosis in renal ischaemia-reperfusion injury by deSUMOylation of HIF-1α.
Article in Journal of cellular and molecular medicine, 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.
- SENP1 drives de novo cholesterogenesis via disrupting SUMOylation-mediated SREBP2-FBXW7 interaction.Cancer & metabolism · 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
- Carfilzomib triggers cardiotoxicity by suppressing SENP1-mediated deSUMOylation of DDX17.Acta biochimica et biophysica Sinica · 2025Article
- SUMOylation of ZEB1 Modulates PANoptosis in Burn-Induced Early Acute Kidney Injury.Journal of cellular and molecular medicine · 2025Article
- High-Resolution Tracking of Aging-Related Small Molecules: Bridging Pollutant Exposure, Brain Aging Mechanisms, and Detection Innovations.Biosensors · 2025Review
- Ferroptosis in ischemia-reperfusion injury: molecular mechanisms and therapeutic strategies.American journal of cardiovascular disease · 2025Review
- Oxidative stress-related genes in uveal melanoma: the role of CALM1 in modulating oxidative stress and apoptosis and its prognostic significance.Frontiers in oncology · 2025Article
- SENP1 reduces oxidative stress and apoptosis in renal ischaemia-reperfusion injury by deSUMOylation of HIF-1α.Journal of cellular and molecular medicine · 2024Article
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Authors and funding
8 authors.
Funding
Abstract
Renal ischaemia-reperfusion injury (RIRI) is a primary cause of acute kidney damage, occurring frequently in situations like renal transplantation, yet the underlying mechanisms were not fully understood. Sentrin-specific protease 1 (SENP1) is an important member of the SENP family, which is widely involved in various diseases. However, the role of SENP1 in RIRI has been unclear. In our study, we discovered that SENP1 was involved in RIRI and reduced renal cell apoptosis and oxidative stress at elevated levels. Further mechanistic studies showed that hypoxia-inducible factor-1α (HIF-1α) was identified as a substrate of SENP1. Furthermore, SENP1 deSUMOylated HIF-1α, which reduced the degradation of HIF-1α, and exerted a renoprotective function. In addition, the protective function was lost after application of the HIF-1α specific inhibitor KC7F2. Briefly, our results fully demonstrated that SENP1 reduced the degradation of HIF-1α and attenuated oxidative stress and apoptosis in RIRI by regulating the deSUMOylation of HIF-1α, suggesting that SENP1 may serve as a potential therapeutic target for the treatment of RIRI.
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