ReviewPediatric nephrology (Berlin, Germany)2015
Macrophage-mediated injury and repair after ischemic kidney injury.
Review in Pediatric nephrology (Berlin, Germany), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 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.
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Who cites it
101 citing papers in PubMed, 161 citations in OpenAlex.
- Macrophage-Fibroblast Crosstalk in Kidney Injury: A Narrative Review.International journal of molecular sciences · 2026Review
- STK40 inhibits profibrotic Arg1Acta pharmacologica Sinica · 2026Article
- When Protection Turns Pathogenic: Dual Compartment Functions of Myeloid YB-1 in Renal IRI.International journal of molecular sciences · 2026Article
- Article
- Predicting Macrophage Spatial Localization from Single-Cell Transcriptomes to Uncover Disease Mechanisms.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Precision nanotherapeutics for kidney disease: targeting inflammation and maladaptive repair.International urology and nephrology · 2026Review
- Elevated FTO alleviates sepsis‑induced acute kidney injury by regulating macrophage inflammatory phenotypes.International journal of molecular medicine · 2026Article
- Unraveling the pleiotropic effects of CCR2-dependent signal transduction in fibrosis development.Theranostics · 2026Review
- AT2R activation reduces M1-type macrophages and promotes tregs accumulation in ischemia-reperfusion-induced acute kidney injury.Frontiers in pharmacology · 2026Article
- The role of ferroptosis in acute kidney injury: the preemptive mode of cell death and the bridging effect.Renal failure · 2025Review
- Non-invasive assessment of activated renal macrophages by imaging of colony-stimulating factor 1 receptor in mouse model with ischemic acute kidney injury.Journal of inflammation (London, England) · 2025Article
- Advances in Nano-Immunomodulatory Systems for the Treatment of Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Exosomes derived from a mesenchymal-like endometrial regenerative cells ameliorate renal ischemia reperfusion injury through delivery of CD73.Stem cell research & therapy · 2025Article
- [Nafamostat Mesylate Alleviates Renal Ischemia-Reperfusion Injury in a Rat Model Through HMGB1 Modulation: An Omics Analysis -Based Study of the Protective Effect and the Mechanisms Involved].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Article
- Diabetic kidney disease: m6A modification as a marker of disease progression and subtype classification.Frontiers in medicine · 2025Article
- The Kidney Precision Medicine Project and Single-Cell Biology of the Injured Proximal Tubule.The American journal of pathology · 2025Review
- Comprehensive analysis of cuproptosis-related genes in immune infiltration and development of a novel diagnostic model for acute kidney injury.Renal failure · 2024Article
- MiR-92a-3p Promotes Renal Injury and Fibrosis Through Facilitating M1 Macrophage Polarization via Targeting LIN28A.Physiological research · 2024Article
- Emodin inhibits M1 macrophage activation that related to acute and chronic kidney injury through EGFR/MAPK pathway.Functional & integrative genomics · 2024Article
- Epithelial CEBPD activates fibronectin and enhances macrophage adhesion in renal ischemia-reperfusion injury.Cell death discovery · 2024Article
41 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Acute ischemic kidney injury is a common complication in hospitalized patients. No treatment is yet available for augmenting kidney repair or preventing progressive kidney fibrosis. Animal models of acute kidney injury demonstrate that activation of the innate immune system plays a major role in the systemic response to ischemia/reperfusion injury. Macrophage depletion studies suggest that macrophages, key participants in the innate immune response, augment the initial injury after reperfusion but also promote tubular repair and contribute to long-term kidney fibrosis after ischemic injury. The distinct functional outcomes seen following macrophage depletion at different time points after ischemia/reperfusion injury suggest heterogeneity in macrophage activation states. Identifying the pathways that regulate the transitions of macrophage activation is thus critical for understanding the mechanisms that govern both macrophage-mediated injury and repair in the postischemic kidney. This review examines our understanding of the complex and intricately controlled pathways that determine monocyte recruitment, macrophage activation, and macrophage effector functions after renal ischemia/reperfusion injury. Careful delineation of repair and resolution pathways could provide therapeutic targets for the development of effective treatments to offer patients with acute kidney injury.
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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.