ArticleAmerican journal of physiology. Renal physiology2013
Macrophages directly mediate diabetic renal injury.
Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.
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Who cites it
96 citing papers in PubMed, 1 synthesis or guideline pooled it, 170 citations in OpenAlex.
- Protective effect of paeoniflorin in diabetic nephropathy: A preclinical systematic review revealing the mechanism of action.PloS one · 2023Pooled it
- Association of environmental xylene exposure with diabetic kidney disease: a cross-sectional analysis and multi-omics evaluation of immune microenvironment mechanisms.Renal failure · 2026Article
- Inflammation and Diabetic Kidney Disease.International journal of molecular sciences · 2026Review
- Differences and significance of macrophage subtypes and regulatory T lymphocytes in the expression of interstitial fibrosis in diabetic nephropathy at different stages.BMC nephrology · 2026Article
- Mesenchymal Stem Cells Polarize Macrophages to an Anti-Inflammatory Phenotype to Ameliorate Diabetic Nephropathy.Stem cells international · 2026Article
- Progress in the study of the role of C5a-induced tubular cell senescence in the progression of diabetic kidney disease.Annals of medicine · 2025Review
- Macrophage polarization in diabetic vascular complications: mechanistic insights and therapeutic targets.Journal of translational medicine · 2025Review
- Macrophage Derived Galectin-3 Promotes Renal Fibrosis and Diabetic Kidney Disease by Enhancing TGFβ1 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Unraveling diabetic kidney disease: insights from single-cell RNA sequencing.International urology and nephrology · 2025Review
- Macrophage Depletion Alleviates Immunosenescence in Diabetic Kidney by Modulating GDF-15 and Klotho.International journal of molecular sciences · 2025Article
- Acute hyperglycemia induces podocyte apoptosis by monocyte TNF-α release, a process attenuated by vitamin D and GLP-1 receptor agonists.The Journal of steroid biochemistry and molecular biology · 2025Article
- REDD1 expression in podocytes facilitates renal inflammation and pyroptosis in streptozotocin-induced diabetic nephropathy.Cell death & disease · 2025Article
- Uncovering glycolysis-driven molecular subtypes in diabetic nephropathy: a WGCNA and machine learning approach for diagnostic precision.Biology direct · 2025Article
- Review
- Mogrosides Protect Against Diabetic Kidney Injury via Inhibiting Macrophage Activation in a Mouse Model.Journal of diabetes research · 2025Article
- M2 macrophage infusion ameliorates diabetic glomerulopathyRenal failure · 2024Article
- The advance of single cell transcriptome to study kidney immune cells in diabetic kidney disease.BMC nephrology · 2024Review
- Fiery Connections: Macrophage-Mediated Inflammation, the Journey from Obesity to Type 2 Diabetes Mellitus and Diabetic Kidney Disease.Biomedicines · 2024Review
- Update on Biomarkers of Chronic Inflammatory Processes Underlying Diabetic Neuropathy.International journal of molecular sciences · 2024Review
- Reconstituted HDL ameliorated renal injury of diabetic kidney disease in mice.Physiological reports · 2024Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Monocyte/macrophage recruitment correlates strongly with the progression of renal impairment in diabetic nephropathy (DN), yet their direct role is not clear. We hypothesized that macrophages contribute to direct podocyte injury and/or an abnormal podocyte niche leading to DN. Experiments were conducted in CD11b-DTR mice treated with diphtheria toxin (DT) to deplete macrophages after streptozotocin-induced diabetes. Additional experiments were conducted in bone marrow chimeric (CD11b-DTR→ C57BL6/J) mice. Diabetes was associated with an increase in the M1-to-M2 ratio by 6 wk after the induction of diabetes. Macrophage depletion in diabetic CD11b-DTR mice significantly attenuated albuminuria, kidney macrophage recruitment, and glomerular histological changes and preserved kidney nephrin and podocin expression compared with diabetic CD11b-DTR mice treated with mutant DT. These data were confirmed in chimeric mice indicating a direct role of bone marrow-derived macrophages in DN. In vitro, podocytes grown in high-glucose media significantly increased macrophage migration compared with podocytes grown in normal glucose media. In addition, classically activated M1 macrophages, but not M2 macrophages, induced podocyte permeability. These findings provide evidence showing that macrophages directly contribute to kidney injury in DN, perhaps by altering podocyte integrity through the proinflammatory M1 subset of macrophages. Attenuating the deleterious effects of macrophages on podocytes could provide a new therapeutic approach to the treatment of DN.
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