ReviewNature reviews. Nephrology2015
Immune cells in experimental acute kidney injury.
Review in Nature reviews. Nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 298 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
298 citing papers in PubMed.
- Single-cell RNA sequencing identifies a proinflammatory S100a8/a9Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Deubiquitinating enzymes in kidney diseases: Molecular mechanisms, pathological roles and therapeutic opportunities (Review).Molecular medicine reports · 2026Review
- Review
- An HRedox biology · 2026Article
- Protective Arm of Renin-Angiotensin System: Evidence of Nephroprotective Effects Against Acute Kidney Injury.Acta physiologica (Oxford, England) · 2026Review
- Systemic immune-inflammation index (SII): a predictor of mortality risk in pediatric acute kidney injury.Pediatric research · 2026Article
- Blood Count-Based Inflammatory Indices Do Not Improve Prediction of Acute Kidney Injury in Cardiogenic Shock.Journal of clinical medicine research · 2026Review
- Alpha-Mangostin in Acute Kidney Injury: Molecular Mechanisms, Regulated Cell Death, and Translational Opportunities.Antioxidants (Basel, Switzerland) · 2026Review
- Bio-hybrid nanovesicles with multimodal antioxidant and immunomodulatory functions attenuate acute kidney injury.Journal of nanobiotechnology · 2026Article
- Tiki2 restrains Wnt5a/Ror signaling to limit inflammation in acute kidney injury.Communications biology · 2026Article
- Brazilin attenuates kidney ischemia-reperfusion injury by regulating inflammation, oxidative stress, and mitochondrial dysfunction.Histology and histopathology · 2026Article
- Impact of ischemia duration on MRI-derived perfusion parameters in a mouse kidney transplant model.European radiology experimental · 2026Article
- Prediction of severe sepsis-associated acute kidney injury incorporating immune-inflammatory profiles: development and validation of a machine learning model in a multicenter prospective cohort study.Frontiers in immunology · 2026Article
- SEC61: a potential therapeutic target in transplantation.Frontiers in immunology · 2026Review
- AT2R activation reduces M1-type macrophages and promotes tregs accumulation in ischemia-reperfusion-induced acute kidney injury.Frontiers in pharmacology · 2026Article
- Immune Infiltration-Related Genes as Potential Biomarkers and Predicted Targets for Renal Allograft Delayed Graft Function and Survival Outcome: An Integrated Machine Learning Approach and Drugs Analysis.Mediators of inflammation · 2026Article
- Total Glucosides of Paeony Alleviates Acute Kidney Injury by Inhibiting Dendritic Cells and T-Cell Communication.Advances in pharmacological and pharmaceutical sciences · 2026Article
- Trem2 activation by renal tubular debris sustains Arg1Frontiers in immunology · 2026Article
- Extracellular vesicles mediate immune regulation in acute kidney injury.Frontiers in immunology · 2026Review
- Macrophage polarization in ischemia-reperfusion injury: from molecular mechanisms to therapeutic strategies.Frontiers in immunology · 2026Review
238 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) prolongs hospital stay and increases mortality in various clinical settings. Ischaemia-reperfusion injury (IRI), nephrotoxic agents and infection leading to sepsis are among the major causes of AKI. Inflammatory responses substantially contribute to the overall renal damage in AKI. Both innate and adaptive immune systems are involved in the inflammatory process occurring in post-ischaemic AKI. Proinflammatory damage-associated molecular patterns, hypoxia-inducible factors, adhesion molecules, dysfunction of the renal vascular endothelium, chemokines, cytokines and Toll-like receptors are involved in the activation and recruitment of immune cells into injured kidneys. Immune cells of both the innate and adaptive immune systems, such as neutrophils, dendritic cells, macrophages and lymphocytes contribute to the pathogenesis of renal injury after IRI, and some of their subpopulations also participate in the repair process. These immune cells are also involved in the pathogenesis of nephrotoxic AKI. Experimental studies of immune cells in AKI have resulted in improved understanding of the immune mechanisms underlying AKI and will be the foundation for development of novel diagnostic and therapeutic targets. This Review describes what is currently known about the function of the immune system in the pathogenesis and repair of ischaemic and nephrotoxic 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 OpenQuestion graph.