ArticleThe Journal of clinical investigation2012
CSF-1 signaling mediates recovery from acute kidney injury.
Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 217 papers, 2 of them syntheses that pooled it.
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
217 citing papers in PubMed, 2 syntheses or guidelines pooled it, 304 citations in OpenAlex.
- Global trends and prospects related to macrophage in chronic kidney disease: a bibliometric analysis.Renal failure · 2024Pooled it
- Macrophages in Renal Injury, Repair, Fibrosis Following Acute Kidney Injury and Targeted Therapy.Frontiers in immunology · 2022Pooled it
- Macrophage-Fibroblast Crosstalk in Kidney Injury: A Narrative Review.International journal of molecular sciences · 2026Review
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- Acute Kidney Injury-to-Chronic Kidney Disease Transition-Associated Macrophage Subtypes: Biological Functions and Intercellular Crosstalk.International journal of molecular sciences · 2026Review
- M2 polarization of macrophages: Manipulation of spinal cord injury repair.Neural regeneration research · 2026Article
- Tissue-Resident Macrophage in Inflammation and Cancer.MedComm · 2026Review
- Bcl-2-Dependent Persistence of Mononuclear Phagocytes Promotes Ocular Fibrosis.International journal of molecular sciences · 2026Article
- Apoptotic Bodies in Kidney Disease: Orchestrators of Inflammation, Fibrosis, and Repair.Journal of the American Society of Nephrology : JASN · 2026Review
- Article
- Spatiotemporal Control of Intercellular Crosstalk: A New Therapeutic Paradigm for Halting Acute Kidney Injury to Chronic Kidney Disease Transition.Biomolecules · 2026Review
- Single-nucleus transcriptomics illuminates sex differences during murine Escherichia coli pyelonephritis.Communications biology · 2026Article
- Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Macrophage Niche Reconstitution Reveals Dynamic Transcriptional and Communication Networks Renal Macrophage-Epithelial Communication.Research square · 2026Article
- Targeting cGAS-STING-macrophage axis: a novel therapeutic horizon for renal fibrosis.Frontiers in immunology · 2026Review
- Single-nucleus transcriptomics illuminates sex differences during murine Escherichia coli pyelonephritis.Research square · 2025Article
- Innate immune cells in acute and chronic kidney disease.Nature reviews. Nephrology · 2025Review
- The crucial role of metabolic reprogramming in driving macrophage conversion in kidney disease.Cellular & molecular biology letters · 2025Review
- Myeloid EGFR deficiency accelerates recovery from AKI via macrophage efferocytosis and neutrophil apoptosis.Nature communications · 2025Article
- The Intestinal Macrophage-Intestinal Stem Cell Axis in Inflammatory Bowel Diseases: From Pathogenesis to Therapy.International journal of molecular sciences · 2025Review
157 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
13 authors at 1 institution in 1 country.
Funding
Abstract
Renal tubule epithelia represent the primary site of damage in acute kidney injury (AKI), a process initiated and propagated by the infiltration of macrophages. Here we investigated the role of resident renal macrophages and dendritic cells in recovery from AKI after ischemia/reperfusion (I/R) injury or a novel diphtheria toxin-induced (DT-induced) model of selective proximal tubule injury in mice. DT-induced AKI was characterized by marked renal proximal tubular cell apoptosis. In both models, macrophage/dendritic cell depletion during the recovery phase increased functional and histologic injury and delayed regeneration. After I/R-induced AKI, there was an early increase in renal macrophages derived from circulating inflammatory (M1) monocytes, followed by accumulation of renal macrophages/dendritic cells with a wound-healing (M2) phenotype. In contrast, DT-induced AKI only generated an increase in M2 cells. In both models, increases in M2 cells resulted largely from in situ proliferation in the kidney. Genetic or pharmacologic inhibition of macrophage colony-stimulating factor (CSF-1) signaling blocked macrophage/dendritic cell proliferation, decreased M2 polarization, and inhibited recovery. These findings demonstrated that CSF-1-mediated expansion and polarization of resident renal macrophages/dendritic cells is an important mechanism mediating renal tubule epithelial regeneration after 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.