ArticleJournal of the American Society of Nephrology : JASN2019
Tubular GM-CSF Promotes Late MCP-1/CCR2-Mediated Fibrosis and Inflammation after Ischemia/Reperfusion Injury.
Article in Journal of the American Society of Nephrology : JASN, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
105 citing papers in PubMed, 1 synthesis or guideline pooled it, 175 citations in OpenAlex.
- Macrophages in Renal Injury, Repair, Fibrosis Following Acute Kidney Injury and Targeted Therapy.Frontiers in immunology · 2022Pooled it
- Targeting a Novel AREGCell proliferation · 2026Article
- T-Cell Remodeling in Renal Fibrosis: From Acute Injury to Chronic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- HMGB1/MYH9 suppresses PPARγ to induce lung injury in renal ischemia-reperfusion: protective effects of Rosiglitazone.Pediatric research · 2026Article
- Synchronization of the 12-h circatidal rhythm maintains the kidney through repeated cycles of warm reperfusion in the hibernating ground squirrel.Function (Oxford, England) · 2026Article
- Inhibiting biofilm growth on ammonium salt-functionalized or fluorinated voice prostheses silicone.Applied microbiology and biotechnology · 2026Article
- ADAM19 participated in peritoneal fibrosis by regulating M2 macrophage polarization in peritoneal dialysis patients.Scientific reports · 2026Article
- CXCR6+ T cells promote apoptosis and necroptosis in proximal tubules during AKI-to-CKD transition.Cell death & disease · 2026Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Applying dendrimer nanoprobes to the diagnosis and evaluation of kidney fibrosis.Nanomedicine (London, England) · 2026Review
- Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Tubule-Derived IFN-α Promotes GSDMD-Mediated Macrophage Pyroptosis to Drive Renal Inflammation and Fibrosis Through JAK2/STAT2 Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Unraveling the pleiotropic effects of CCR2-dependent signal transduction in fibrosis development.Theranostics · 2026Review
- Comparison of the effects of direct and remote ischemic post and preconditioning in the kidney of young rats: histological and laboratory evaluation.Acta cirurgica brasileira · 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
- Design of precision therapeutics for a CKD risk allele by targeting Shroom3-Rock interaction.Nature communications · 2025Article
- Multi-omics analysis of host airway responses in pediatric Mycoplasma pneumoniae pneumonia reveals potential mechanisms of disease exacerbation caused by co-infection.NPJ biofilms and microbiomes · 2025Article
- Piezo1 aggravates ischemia/reperfusion-induced acute kidney injury by CaRenal failure · 2025Article
- Crosstalk between macrophages and adjacent cells in AKI to CKD transition.Renal failure · 2025Review
- Myeloid Cells in Acute Kidney Injury.Seminars in nephrology · 2025Review
45 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
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAfter bilateral kidney ischemia/reperfusion injury (IRI), monocytes infiltrate the kidney and differentiate into proinflammatory macrophages in response to the initial kidney damage, and then transition to a form that promotes kidney repair. In the setting of unilateral IRI (U-IRI), however, we have previously shown that macrophages persist beyond the time of repair and may promote fibrosis.
methodsMacrophage homing/survival signals were determined at 14 days after injury in mice subjected to U-IRI and
resultsFailure to resolve tubular injury after U-IRI results in sustained expression of granulocyte-macrophage colony-stimulating factor by renal tubular cells, which directly stimulates expression of monocyte chemoattractant protein-1 (
conclusionsGM-CSF-induced MCP-1/CCR2 signaling plays an important role in the cross-talk between injured tubular cells and infiltrating immune cells and myofibroblasts, and promotes sustained inflammation and tubular injury with progressive interstitial fibrosis in the late stages of U-IRI.
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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.