ArticleInflammation2025
Dexmedetomidine Alleviates Acute Stress-Induced Acute Kidney Injury by Attenuating Inflammation and Oxidative Stress via Inhibiting the P2X
Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- P2X7 receptor: a potential therapeutic target for chronic respiratory diseases.Molecular and cellular biochemistry · 2026Review
- ATP-P2X7R-NLRP3 Axis as a Unifying Mechanism of ATP-Induced Cell Death in Degenerative Bone and Cardiovascular Diseases.Journal of inflammation research · 2026Review
- Single-Cell RNA-Seq Revealed the Immune Microenvironment Reprogramming by Dexmedetomidine Treatment in Ischemic Stroke.Molecular neurobiology · 2025Article
- Dexmedetomidine-Loaded Hydrogel Microneedles Alleviate Acute Inflammatory Visceral Pain in Mice.Gels (Basel, Switzerland) · 2025Article
- Network expression analysis identifies and experimentally validates the involvement of Fosb in acute kidney injury.FASEB bioAdvances · 2025Article
- Dexmedetomidine improves clinical outcomes in sepsis-induced myocardial injury: a retrospective cohort study.Frontiers in pharmacology · 2024Article
- Dexmedetomidine regulates the anti-oxidation and autophagy of adipose-derived stromal cells under HFrontiers in pharmacology · 2024Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
This study aimed to investigate the potential protective effects of Dexmedetomidine (DEX) against acute kidney injury (AKI) induced by acute stress (AS). Wistar rats were divided into five groups: Control, DEX, AS, AS + DEX, and AS + A438079. The results showed that AS led to AKI by increasing inflammatory biomarkers and oxidative stress-related indicators. The acute stress model in rats was successfully established. Renal function, histopathology, oxidative stress, and inflammation were assessed. Localization of P2X7 receptor (P2X7R) was determined by immunofluorescence. Additionally, the key inflammatory proteins of the P2X7R/NF-κB/NLRP3 signaling pathway were measured by Western blotting. DEX significantly improved kidney function, alleviated kidney injury, and reduced oxidative stress and inflammation. DEX inhibited the activation of the P2X7R, decreased the expression of NF-κB, NLRP3 inflammasome, and Caspase-1, and inhibited the expression of interleukin-1β (IL-1β) and tumor necrosis factor α (TNFα). Furthermore, DEX also alleviated AS-induced AKI by inhibiting the excessive production of reactive oxygen species (ROS) and reducing oxidative stress. In conclusion, DEX attenuates AS-induced AKI by mitigating inflammation and oxidative stress through the inhibition of the P2X7R/NF-κB/NLRP3 pathway in rats.
Indexed as
Identifiers
38896231What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.