ArticleKidney international2015
Proximal tubule-derived colony stimulating factor-1 mediates polarization of renal macrophages and dendritic cells, and recovery in acute kidney injury.
Article in Kidney international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 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
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Who cites it
61 citing papers in PubMed, 101 citations in OpenAlex.
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- Tourniquet Duration and Early Clinical and Biomarker Outcomes in Total Knee Arthroplasty: A Comparative Cohort Study.Journal of clinical medicine · 2026Article
- Shared multicellular injury programs of acute and chronic kidney disease enable mechanistic patient stratification.medRxiv : the preprint server for health sciences · 2026Article
- Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026Review
- BMAL1 regulates tubular epithelial-derived exosomal miR-27a-3p to inhibit macrophage-myofibroblast transition and alleviate ischemia/reperfusion-induced renal fibrosis.Theranostics · 2026Article
- Crosstalk between macrophages and adjacent cells in AKI to CKD transition.Renal failure · 2025Review
- Cage-Farming Causes Histopathological Alterations in the Renal Tissues of the Rainbow TroutInternational journal of molecular sciences · 2025Article
- Exercise sensitizes the pressure diuresis response: shifting immune landscapes may underlie renal adaptations.American journal of physiology. Renal physiology · 2025Article
- 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
- Adding insult to injury: the spectrum of tubulointerstitial responses in acute kidney injury.The Journal of clinical investigation · 2025Review
- Tissue-resident macrophages and renal diseases: landscapes and treatment directions.Frontiers in immunology · 2025Review
- Review
- Identification of key genes in membranous nephropathy and non-alcoholic fatty liver disease by bioinformatics and machine learning.Frontiers in immunology · 2025Article
- Spatial transcriptomics defines injury specific microenvironments and cellular interactions in kidney regeneration and disease.Nature communications · 2024Article
- Epigenetic reprogramming driving successful and failed repair in acute kidney injury.Science advances · 2024Article
- Epigenetic reprogramming driving successful and failed repair in acute kidney injury.bioRxiv : the preprint server for biology · 2024Article
- Cellular cross-talk drives mesenchymal transdifferentiation in diabetic kidney disease.Frontiers in medicine · 2024Review
- Exploring Cuproptosis-Related Genes and Diagnostic Models in Renal Ischemia-Reperfusion Injury Using Bioinformatics, Machine Learning, and Experimental Validation.Journal of inflammation research · 2024Article
- Spatial transcriptomics defines injury-specific microenvironments in the adult mouse kidney and novel cellular interactions in regeneration and disease.bioRxiv : the preprint server for biology · 2023Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Infiltrating cells play an important role in both the development of and recovery from acute kidney injury (AKI). Macrophages and renal dendritic cells are of particular interest because they can exhibit distinctly different functional phenotypes, broadly characterized as proinflammatory (M1) or tissue reparative (M2). Resident renal macrophages and dendritic cells participate in recovery from AKI in response to either ischemia/reperfusion or a model of selective proximal tubule injury induced by diphtheria-toxin-induced apoptosis in transgenic mice expressing the human diphtheria toxin receptor on proximal tubule cells. Colony-stimulating factor-1 (CSF-1) is an important factor mediating the recovery from AKI, and CSF-1 can stimulate macrophage and dendritic cell proliferation and polarization during the recovery phase of AKI. The kidney, and specifically the proximal tubule, is a major source of intrarenal CSF-1 production in response to AKI. We induced selective deletion of proximal tubule CSF-1 to determine its role in expansion and proliferation of renal macrophages and dendritic cells and in recovery from AKI. In both models of AKI, there was decreased M2 polarization, delayed functional and structural recovery, and increased tubulointerstitial fibrosis. Thus, intrarenal CSF-1 is an important mediator of macrophage/dendritic cell polarization and recovery from AKI.
Identifiers
What OpenQuestion holds
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.