ArticleMolecular medicine (Cambridge, Mass.)2024
Dexmedetomidine ameliorates acute kidney injury by regulating mitochondrial dynamics via the α2-AR/SIRT1/PGC-1α pathway activation in rats.
Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Safety and efficacy of dexmedetomidine in combination with ropivacaine for lumbar paravertebral block in posterior lumbar surgery: a randomized controlled trial.BMC anesthesiology · 2026Trial
- Renoprotective Effects of a Herbal Formulation Against Lipopolysaccharide-Induced Acute Kidney Injury Through Anti-Inflammatory and Antioxidant Activities.Life (Basel, Switzerland) · 2026Article
- Pediatric sepsis-associated acute kidney injury: leveraging pathophysiology for risk stratification and identification of treatable traits.Pediatric nephrology (Berlin, Germany) · 2026Review
- Sophocarpine Alleviates Renal Ischemia-Reperfusion Injury by Mitigating Oxidative Stress and Mitochondrial Dysfunction via the SIRT1/PGC-1α Axis.Biomedicines · 2026Article
- Role of oxidative stress in sepsis: Mechanisms, pathways, and therapeutic strategies.Journal of pharmaceutical analysis · 2026Review
- Bridging tradition and modernity: mitochondrial dynamics as a Traditional Chinese Medicine therapeutic target in cardiovascular disease.Chinese medicine · 2026Review
- CaMKII phosphorylation promotes renal fibrosis in cisplatin induced chronic kidney disease via Smad 2/3 activation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Dexmedetomidine reduces acute kidney injury in high-risk but not low-risk patients after non-cardiac surgery: secondary analysis of a randomized controlled trial.Journal of anesthesia · 2026Article
- Calcium homeostasis imbalance in sepsis: molecular mechanisms and therapeutic perspectives.Frontiers in medicine · 2026Review
- Mitochondrial calcium uniporter-mediated mitochondrial dynamics imbalance contributes to contrast medium-induced renal tubular cell injury.Frontiers in molecular biosciences · 2026Article
- Mitochondrial fission and fusion in inflammatory diseases: mechanisms and therapeutic implications.Journal of translational medicine · 2025Review
- Sirtuin Family in Acute Kidney Injury: Insights into Cellular Mechanisms and Potential Targets for Treatment.Biomolecules · 2025Review
- Integrin CD11b Alleviates Cerebral Ischemia/Reperfusion Injury via a Mechanism Involving Microglia/Macrophage Polarization.Journal of molecular neuroscience : MN · 2025Article
- Melatonin Alleviates MBP-Induced Oxidative Stress and Apoptosis in TM3 Cells via the SIRT1/PGC-1α Signaling Pathway.International journal of molecular sciences · 2025Article
- Mechanisms of alveolar type II epithelial cells' mitochondrial quality control during acute lung injury/acute respiratory distress syndrome: bridging the gap between oxidative stress, inflammation, and fibrosis.Frontiers in physiology · 2025Review
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Authors and funding
19 authors.
Funding
Abstract
backgroundSepsis-associated acute kidney injury (AKI) is a serious complication of systemic infection with high morbidity and mortality in patients. However, no effective drugs are available for AKI treatment. Dexmedetomidine (DEX) is an alpha 2 adrenal receptor agonist with antioxidant and anti-apoptotic effects. This study aimed to investigate the therapeutic effects of DEX on sepsis-associated AKI and to elucidate the role of mitochondrial dynamics during this process.
methodsA lipopolysaccharide (LPS)-induced AKI rat model and an NRK-52E cell model were used in the study. This study investigated the effects of DEX on sepsis-associated AKI and the molecular mechanisms using histologic assessment, biochemical analyses, ultrastructural observation, western blotting, immunofluorescence, immunohistochemistry, qRT-PCR, flow cytometry, and si-mRNA transfection.
resultsIn rats, the results showed that administration of DEX protected kidney structure and function from LPS-induced septic AKI. In addition, we found that DEX upregulated the α2-AR/SIRT1/PGC-1α pathway, protected mitochondrial structure and function, and decreased oxidative stress and apoptosis compared to the LPS group. In NRK-52E cells, DEX regulated the mitochondrial dynamic balance by preventing intracellular Ca
conclusionsDEX ameliorated septic AKI by reducing oxidative stress and apoptosis in addition to modulating mitochondrial dynamics via upregulation of the α2-AR/SIRT1/PGC-1α pathway. This is a confirmatory study about DEX pre-treatment to ameliorate septic AKI. Our research reveals a novel mechanistic molecular pathway by which DEX provides nephroprotection.
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