ArticleJournal of inflammation research2023
Neutrophil Extracellular Traps Aggravate Contrast-Induced Acute Kidney Injury by Damaging Glomeruli and Peritubular Capillaries.
Article in Journal of inflammation research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed.
- Basophil Extracellular Traps in Immunity and Disease.Cancers · 2026Review
- Neutrophil Extracellular Traps Exacerbate UVB-Induced Photodamage in HaCaT Cells and Mouse Skin via CCDC25/MAPK Pathway.Aging cell · 2026Article
- Bionic black phosphorus nanosheets confer dual protection against nephrocalcinosis-induced kidney injury via ROS scavenging and NETosis inhibition.Materials today. Bio · 2026Article
- Spatiotemporal Control of Intercellular Crosstalk: A New Therapeutic Paradigm for Halting Acute Kidney Injury to Chronic Kidney Disease Transition.Biomolecules · 2026Review
- Citrate-coated Prussian blue nanozyme hitchhikes neutrophils to ameliorate calcium oxalate crystal-induced kidney injury via inhibiting pyroptosis and NETosis.Journal of nanobiotechnology · 2026Article
- Study on the pro-inflammatory injury of neutrophil extracellular traps in gouty nephropathy.Frontiers in immunology · 2026Review
- Neutrophils in Kidney Disease: Linking Neutrophil Function and Microenvironment to Therapeutic Targets.Journal of inflammation research · 2026Review
- Mac-1 Promotes Neutrophil Extracellular Traps Formation via ERK Phosphorylation in Renal Ischemia-Reperfusion Injury.Inflammation · 2025Article
- Toll Like Receptors Promote High Glucose-Induced Vascular Endothelial Cell Dysfunction by Regulating Neutrophil Extracellular Traps Formation.Inflammation · 2025Article
- CitH3, a Druggable Biomarker for Human Diseases Associated with Acute NETosis and Chronic Immune Dysfunction.Pharmaceutics · 2025Review
- Establishing a Predictive Model for the Occurrence of CI-AKI After PCI in Patients With Coronary Heart Disease Based on Serum-Derived Biomarkers.Cardiology research and practice · 2025Article
- Hypertension and BMI as Mediators of Type 2 Diabetes-Induced CKD: Insights from an Integrative Multi-Database Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Neutrophil and neutrophil extracellular traps in acute kidney injury: from mechanisms to treatments.Frontiers in immunology · 2025Review
- DNase I alleviates renal inflammatory injury in MRL/lpr mice by inhibiting NETs formation.Frontiers in immunology · 2025Article
- Role of Neutrophil Extracellular Traps in Hypertension and Their Impact on Target Organs.Journal of clinical hypertension (Greenwich, Conn.) · 2025Review
- Review of research progress in sepsis-associated acute kidney injury.Frontiers in molecular biosciences · 2025Review
- Development and Testing a New Online Dynamic Nomogram for Contrast-Induced Acute Kidney Injury in Elderly Patients with ST-Segment Elevation Myocardial Infarction.Clinical interventions in aging · 2025Article
- The Protective Role of Intermedin in Contrast-Induced Acute Kidney Injury: Enhancing Peritubular Capillary Endothelial Cell Adhesion and Integrity Through the cAMP/Rac1 Pathway.International journal of molecular sciences · 2024Article
- Association of corticosteroid therapy with reduced acute kidney injury and lower NET markers in severe COVID-19: an observational study.Intensive care medicine experimental · 2024Article
- Unveiling the Mysteries of Contrast-Induced Acute Kidney Injury: New Horizons in Pathogenesis and Prevention.Toxics · 2024Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Contrast-induced acute kidney injury (CI-AKI) is considered to be the third leading cause of hospital-acquired kidney injury. Current studies mostly suggest that contrast agents mainly harm renal tubular epithelial cells, but we hypothesized that the development of CI-AKI should be the result of the interaction of renal vascular and tubular injury. Methods: First we constructed a CI-AKI mouse model and verified the success of the model by pathological injury and serum creatinine level. Immunohistochemistry, protein quantification and qRT-PCR were used to detect the location and level of expression of neutrophil extracellular traps (NETs) in the kidney. Then, we blocked the in vivo accumulation of NETs using GSK484 and DNase I and detected the expression of NETs and the damage of glomerular and peritubular capillaries. Results: We first identified the presence of NETs in CI-AKI mice, and NETs were mainly accumulated in glomeruli and peritubular capillaries. The expression of NETs was positively correlated with the severity of CI-AKI kidney. After inhibition of NETs release or promotion of NETs degradation by drugs, renal vascular endothelial cell injury was reduced and renal pathological changes and creatinine levels were reversed in CI-AKI mice. In addition, inhibition of NETs reduced apoptosis and pyroptosis of renal cells and attenuated inflammation in vivo. Conclusion: These findings suggest that NETs are involved in the development of CI-AKI by damaging glomerular and peritubular capillary endothelial cells. This study will provide a new strategy for clinical prevention and treatment of CI-AKI.
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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.