ReviewClinical and experimental nephrology2009
Chemokine/chemokine receptor-mediated inflammation regulates pathologic changes from acute kidney injury to chronic kidney disease.
Review in Clinical and experimental nephrology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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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.
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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
46 citing papers in PubMed, 100 citations in OpenAlex.
- Adenine-induced animal model of chronic kidney disease: current applications and future perspectives.Renal failure · 2024Review
- Calcitriol Reduces the Inflammation, Endothelial Damage and Oxidative Stress in AKI Caused by Cisplatin.International journal of molecular sciences · 2022Article
- Extracellular CIRP induces acute kidney injury via endothelial TREM-1.Frontiers in physiology · 2022Article
- Clec7a expression in inflammatory macrophages orchestrates progression of acute kidney injury.Frontiers in immunology · 2022Article
- Decoding the Mechanism behind the Pathogenesis of the Focal Segmental Glomerulosclerosis.Computational and mathematical methods in medicine · 2022Article
- Review
- Prostate-Specific Membrane Antigen and Esterase Dual Responsive Camptothecin-Oligopeptide Self-Assembled Nanoparticles for Efficient Anticancer Drug Delivery.International journal of nanomedicine · 2021Article
- Relationship between the location of ligamentum flavum hypertrophy and its stress in finite element analysis.Orthopaedic surgery · 2020Article
- The Nephroprotective Effect of TNF Receptor-Associated Factor 6 (TRAF6) Blockade on LPS-Induced Acute Renal Injury Through the Inhibition if Inflammation and Oxidative Stress.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Neuroimmune Mechanisms in Signaling of Pain During Acute Kidney Injury (AKI).Frontiers in medicine · 2020Review
- AZD4547 Attenuates Lipopolysaccharide-Induced Acute Kidney Injury by Inhibiting Inflammation: The Role of FGFR1 in Renal Tubular Epithelial Cells.Drug design, development and therapy · 2020Article
- Role of Chemokine (C-X-C Motif) Ligand 10 (CXCL10) in Renal Diseases.Mediators of inflammation · 2020Review
- Article
- Bioactive Compounds for the Treatment of Renal Disease.Yonsei medical journal · 2018Review
- CCR2 contributes to the recruitment of monocytes and leads to kidney inflammation and fibrosis development.Inflammopharmacology · 2018Article
- CX3CL1/CX3CR1 Axis, as the Therapeutic Potential in Renal Diseases: Friend or Foe?Current gene therapy · 2017Review
- Analysis of the Relationship between Ligamentum Flavum Thickening and Lumbar Segmental Instability, Disc Degeneration, and Facet Joint Osteoarthritis in Lumbar Spinal Stenosis.Asian spine journal · 2016Article
- Delivery of interleukin-10 via injectable hydrogels improves renal outcomes and reduces systemic inflammation following ischemic acute kidney injury in mice.American journal of physiology. Renal physiology · 2016Article
- Late intervention with the small molecule BB3 mitigates postischemic kidney injury.American journal of physiology. Renal physiology · 2016Article
- Antiaging Gene Klotho Regulates Adrenal CYP11B2 Expression and Aldosterone Synthesis.Journal of the American Society of Nephrology : JASN · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemia-reperfusion injury is a main cause of acute kidney injury. Tubular necrosis and interstitial inflammatory cell infiltration are characteristic pathologic changes of acute kidney injury. The main necrotic area should be repaired with new tubular epithelial cells after the injury. On the other hand, some parts of the injured kidney progress to interstitial fibrosis, a characteristic pathologic change in chronic kidney disease. We hypothesized that interstitial infiltrating leukocytes, that are attracted and activated by chemokines, are key mediators in the pathogenesis of tubular necrosis, regeneration of the necrotic area, or interstitial fibrosis. A large number of chemokines were upregulated after ischemic injury, and chemokine receptor-expressing inflammatory cells were attracted by these chemokines. Genetic or molecular modulating experiments in the mouse model have begun to reveal the key participants and their specific roles at the levels of inflammation, regeneration, and fibrosis. Among these chemokines/chemokine receptors, our data indicated CCR2-mediated macrophage infiltration mainly affected tubular necrosis after ischemic acute kidney injury, interferon-gamma-inducible protein (IP)-10-producing macrophages participate in regeneration of tubular epithelial cells, and CX3CR1-mediated macrophages and platelet infiltration and aggregation play roles in interstitial fibrosis in chronic kidney disease. These chemokines and chemokine receptors on infiltrating inflammatory cells would be novel clinical markers or targets for therapeutic intervention.
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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 OpenQuestion graph.