ArticleScientific reports2016
M1/M2-macrophage phenotypes regulate renal calcium oxalate crystal development.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 2 of them syntheses that pooled it.
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Who cites it
79 citing papers in PubMed, 2 syntheses or guidelines pooled it, 124 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
- Article
- Inducing bacterial calcification for systematic treatment and immunomodulation against methicillin-resistant Staphylococcus aureus.Nature biotechnology · 2026Article
- GAS5 mediates notch signaling to exacerbate calcium oxalate-induced renal injury through the NF-κB/NLRP3 axis by promoting macrophage polarization.Cellular and molecular life sciences : CMLS · 2026Article
- M2 Macrophages Attenuate AQP2Research (Washington, D.C.) · 2026Article
- The role of inflammation and ROS in CaOx kidney stones.European journal of medical research · 2025Review
- Genetically predicted Circulating inflammatory proteins mediate the association between plasma lipidome and kidney stones: A Mendelian randomization study.Urolithiasis · 2025Article
- Bardoxolone methyl (Bard)-mediated strong suppression of calcium oxalate crystal formation in renal crystal recurrence model.Scientific reports · 2025Article
- Role of UropathogenicPathogens (Basel, Switzerland) · 2025Review
- Scanning electron microscopy and energy dispersive spectroscopy of Randall's plaque stones: an unexpected finding of monosodium urate crystals.Urolithiasis · 2025Article
- Genetically predicted blood metabolites mediate the association between immune cell characteristics and urolithiasis: A Mendelian randomization study and mediation analysis.Genes & diseases · 2025Article
- Apoptosis, ferroptosis, necrosis, necroptosis and pyroptosis in the formation of calcium oxalate kidney stones.Urolithiasis · 2025Review
- 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
- Differences in macrophage pyroptosis and polarization induced by nano-/micro-calcium oxalate crystals.Journal of nanobiotechnology · 2025Article
- Oxidative stress, inflammation and kidney stones.Urolithiasis · 2025Article
- NLRP3 inflammasome activation and macrophage distribution in kidney tissues from patients with acute oxalate nephropathy.Kidney research and clinical practice · 2025Article
- Identification of aging-related biomarkers and immune infiltration analysis in renal stones by integrated bioinformatics analysis.Scientific reports · 2025Article
19 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In our previous report, M2-macrophage (Mφs) deficient mice showed increased renal calcium oxalate (CaOx) crystal formation; however, the role of Mφs-related-cytokines and chemokines that affect kidney stone formation remains unknown. Here, we investigated the role of M1/M2s in crystal development by using in vitro and in vivo approaches. The crystal phagocytic rate of bone marrow-derived M2Mφs was higher than that of bone marrow-derived Mφs and M1Mφs and increased on co-culture with renal tubular cells (RTCs). However, the amount of crystal attachment on RTCs reduced on co-culture with M2Mφs. In six hyperoxaluric C57BL/6J mice, M1Mφ transfusion and induction by LPS and IFN-γ facilitated renal crystal formation, whereas M2Mφ transfusion and induction by IL-4 and IL-13 suppressed renal crystal formation compared with the control. These M2Mφ treatments reduced the expression of crystal-related genes, such as osteopontin and CD44, whereas M1Mφ treatment increased the expression of pro-inflammatory and adhesion-related genes such as IL-6, inducible NOS, TNF-α, C3, and VCAM-1. The expression of M2Mφ-related genes was lower whereas that of M1Mφ-related genes was higher in papillary tissue of CaOx stone formers. Overall, our results suggest that renal crystal development is facilitated by M1Mφs, but suppressed by M2Mφs.
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