ArticleJournal of the American Society of Nephrology : JASN2014
Colony-stimulating factor-1 signaling suppresses renal crystal formation.
Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 2 of them syntheses that pooled it.
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Who cites it
54 citing papers in PubMed, 2 syntheses or guidelines pooled it, 76 citations in OpenAlex.
- Metabolic changes in kidney stone disease.Frontiers in immunology · 2023Pooled it
- Macrophage Function in Calcium Oxalate Kidney Stone Formation: A Systematic Review of Literature.Frontiers in immunology · 2021Pooled it
- Novel insights into the role of the renal interstitial microenvironment in Randall's plaque formation (Review).International journal of molecular medicine · 2026Review
- Phosphaturia Exacerbates Tubular Injury and Cyst Formation in Polycystic Kidney Disease.Kidney360 · 2026Article
- Steroid hormones and nephrolithiasis: regulation of urine components metabolism and inflammation.Biology of sex differences · 2026Review
- Crosstalk between macrophages and adjacent cells in AKI to CKD transition.Renal failure · 2025Review
- Causal Associations of Cardiovascular Proteins and Diabetic Nephropathy Revealed by Mediation and Phenome-Wide Mendelian Randomization.Endocrinology and metabolism (Seoul, Korea) · 2025Article
- Associations of genetic proxies for non-steroidal anti-inflammatory drugs with increased kidney stone risk: a Mendelian randomization study.Inflammopharmacology · 2025Article
- Macrophage Reprogramming: Emerging Molecular Therapeutic Strategies for Nephrolithiasis.Biomolecules · 2025Review
- Comprehensive Mendelian randomization analysis and experimental investigation identifies the causal relationship between immunity and kidney stone disease.Urolithiasis · 2025Article
- The role of osteopontin in modulating macrophage phagocytosis of calcium oxalate crystals.Urolithiasis · 2025Article
- Premature renal epithelial cell senescence promoted by LXN/Rps3/p53 signaling pathway activation increases calcium oxalate crystal deposition by altering macrophage polarization.Frontiers in immunology · 2025Article
- Suppression of renal crystal formation, inflammation, and fibrosis by blocking oncostatin M receptor β signaling.Scientific reports · 2024Article
- Review
- Phagocytosis model of calcium oxalate monohydrate crystals generated using human induced pluripotent stem cell-derived macrophages.Urolithiasis · 2024Article
- Inflammatory factors and the risk of urolithiasis: a bidirectional Mendelian randomization study.Frontiers in medicine · 2024Article
- A bibliometric analysis: CaFrontiers in immunology · 2023Review
- Bioinformatics analysis reveals the potential role of matrix metalloproteinases in immunity and urolithiasis.Frontiers in immunology · 2023Article
- Identification of the core genes in Randall's plaque of kidney stone and immune infiltration with WGCNA network.Frontiers in genetics · 2023Article
- Hydroxyproline stimulates inflammation and reprograms macrophage signaling in a rat kidney stone model.Biochimica et biophysica acta. Molecular basis of disease · 2022Article
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We recently reported evidence suggesting that migrating macrophages (Mϕs) eliminate renal crystals in hyperoxaluric mice. Mϕs can be inflammatory (M1) or anti-inflammatory (M2), and colony-stimulating factor-1 (CSF-1) mediates polarization to the M2Mϕ phenotype. M2Mϕs promote renal tissue repair and regeneration, but it is not clear whether these cells are involved in suppressing renal crystal formation. We investigated the role of M2Mϕs in renal crystal formation during hyperoxaluria using CSF-1-deficient mice, which lack M2Mϕs. Compared with wild-type mice, CSF-1-deficient mice had significantly higher amounts of renal calcium oxalate crystal deposition. Treatment with recombinant human CSF-1 increased the expression of M2-related genes and markedly decreased the number of renal crystals in both CSF-1-deficient and wild-type mice. Flow cytometry of sorted renal Mϕs showed that CSF-1 deficiency resulted in a smaller population of CD11b(+)F4/80(+)CD163(+)CD206(hi) cells, which represent M2-like Mϕs. Additionally, transfusion of M2Mϕs into CSF-1-deficient mice suppressed renal crystal deposition. In vitro phagocytosis assays with calcium oxalate monohydrate crystals showed a higher rate of crystal phagocytosis by M2-polarized Mϕs than M1-polarized Mϕs or renal tubular cells. Gene array profiling showed that CSF-1 deficiency resulted in disordered M2- and stone-related gene expressions. Collectively, our results provide compelling evidence for a suppressive role of CSF-1 signaling in renal crystal formation.
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