ArticleRedox report : communications in free radical research2024
Dexmedetomidine inhibits ferroptosis and attenuates sepsis-induced acute kidney injury via activating the Nrf2/SLC7A11/FSP1/CoQ10 pathway.
Article in Redox report : communications in free radical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Targeting integrated cell death networks in sepsis‑associated acute kidney injury: Shared regulatory nodes and diet‑related small molecule modulation (Review).International journal of molecular medicine · 2026Review
- Ferroptosis in kidney disease.Nature reviews. Nephrology · 2026Review
- Multiple organ dysfunction syndrome: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Crosstalk between autophagy and ferroptosis in diabetes.Genes & diseases · 2026Review
- Protective Effects of Dexmedetomidine Against Ischemic Heart Disease and Diabetic Cardiomyopathy by Targeting Ferroptosis.Reviews in cardiovascular medicine · 2026Review
- Probiotic interventions maintain intestinal barrier function and alleviate necrotizing enterocolitis by inhibiting ferroptosis in intestinal PMN-MDSCs.Cell death & disease · 2026Article
- The role and mechanism of TNFRSF21 in promoting necroptosis of vascular endothelial cells and inducing vascular leakage in sepsis.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Acute kidney injury over the past decade: from definition evolution to pathogenesis insights and innovative therapeutic strategies.Cellular and molecular life sciences : CMLS · 2026Review
- Ferroptosis and immunity: rewiring the tumor microenvironment for therapy.RSC advances · 2026Review
- Non-apoptotic Regulated Cell Death Mechanisms in Sepsis and their Therapeutic Potential.Inflammation · 2026Review
- Dexmedetomidine alleviates sepsis-associated acute kidney injury by inhibiting renal tubular ferroptosis via JNK/MAPK-LCN2 pathway.European journal of medical research · 2026Article
- Magnolol Ameliorates Cisplatin-Induced Acute Kidney Injury with Activation of Nrf2-Associated Antioxidant Responses.Current issues in molecular biology · 2026Article
- Targeting Ferroptosis in Sepsis: Therapeutic Potential and Mechanisms of Natural Products and Traditional Chinese Medicine.Journal of inflammation research · 2026Review
- Inflammation, cell death, and lncRNAs: unraveling the mechanisms of sepsis-associated acute kidney injury.Frontiers in immunology · 2026Review
- Ferroptosis suppressor protein 1-mediated ferroptosis suppression in sepsis: non-canonical antioxidant pathways, inflammatory regulation, and therapeutic perspectives.Frontiers in immunology · 2026Review
- Visnagin Protects Against Lipopolysaccharide-Induced Acute Kidney Injury by Inhibiting Oxidative Stress and Reducing Ferroptosis.International journal of medical sciences · 2026Article
- Dexmedetomidine alleviates ferroptosis caused by traumatic brain injury via the NRF2/HO-1/GPX4 pathway.Metabolic brain disease · 2025Article
- Sepsis-Related Cardiomyopathy: Advances in Diagnosis and Treatment.Reviews in cardiovascular medicine · 2025Review
- Protective Effect of Hepcidin on Sepsis-Associated Acute Kidney Injury via Activating the Nrf2/GPX4 Signaling Pathway.Current issues in molecular biology · 2025Article
- Unveiling the renoprotective mechanisms of self-assembled herbal nanoparticles fromActa pharmaceutica Sinica. B · 2025Article
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Abstract
objectivesThe molecular mechanism underlying the protective effects of DEX against sepsis-induced acute kidney injury (SAKI) remains to be elucidated.
methodsWe established S-AKI models in vivo via CLP and in vitro with LPS-induced HK-2 cells.
resultsThe Nrf2/SLC7A11/FSP1/CoQ10 pathway was inhibited in S-AKI both in vitro and in vivo. The overexpression of Nrf2 inhibited LPS-induced ferroptosis by activating the SLC7A11/FSP1/CoQ10 pathway. DEX ameliorated kidney tissue damage, as determined by a decrease in BUN, Cr, and inflammatory factor levels, along with renal tubule vacuolation and inflammatory cell infiltration in S-AKI mice. Additionally, DEX treatment significantly ameliorated ferroptosis in S-AKI in vitro and in vivo, as indicated by an improvement in mitochondrial shrinkage and disruption of cristae, a decrease in iron, ROS, MDA, and 4-HNE levels, and an increase in GSH and GPX4 levels. Mechanistically, DEX treatment restored the reduction of Nrf2 expression and nuclear translocation in S-AKI, as well as, the levels of downstream SLC7A11, FSP1, and CoQ10. Knocking down Nrf2 in vitro and administering brusatol in vivo eliminated the protective effect of DEX against S-AKI.
conclusionsDEX mitigated ferroptosis and attenuated S-AKI by activating the Nrf2/SLC7A11/FSP1/CoQ10 pathway. Abbreviation: CLP: Cecal ligation puncture; LPS: Lipopolysaccharide; Nrf2: Nuclear factor-erythroid- 2-related factor 2; SLC7A11: Solute carrier family 7 member 11; FSP1: Ferroptosis suppressor protein 1; CoQ10: Coenzyme Q10; BUN: Blood urea nitrogen; Cr: Serum creatinine; ROS: Reactive oxygen species; MDA: Malondialdehyde; 4-HNE: 4-hydroxynonenal; GSH: Hlutathione; GPX4: Glutathione peroxidase 4.
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