ArticleKidney international2006
Monocyte chemoattractant protein-1 promotes the development of diabetic renal injury in streptozotocin-treated mice.
Article in Kidney international, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01847313 (Phase 3 Study of the Effect of Glucagon-like-peptide 1), which is not on this map. Cited by 199 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Phase 3 Study of the Effect of Glucagon-like-peptide 1 (GLP-1) Receptor Agonism on Renal Outcomes in Humans With Diabetic Kidney Disease
Who cites it
199 citing papers in PubMed, 438 citations in OpenAlex.
- C-C motif-ligand 2 inhibition with emapticap pegol (NOX-E36) in type 2 diabetic patients with albuminuria.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2017Trial
- Cilostazol effectively attenuates deterioration of albuminuria in patients with type 2 diabetes: a randomized, placebo-controlled trial.Endocrine · 2014Trial
- Reduced albuminuria with sarpogrelate is accompanied by a decrease in monocyte chemoattractant protein-1 levels in type 2 diabetes.Clinical journal of the American Society of Nephrology : CJASN · 2008Trial
- The association between pan-immune-inflammation value and diabetic kidney disease: a combined cross-sectional and prospective cohort study.BMC endocrine disorders · 2026Article
- Kidney-Vascular Metabolic Crosstalk: Altered Lipoproteins in CKD.Circulation research · 2026Review
- Association of BMI Change with New-Onset or Progressive Diabetic Kidney Disease in People with Normal-Weight Type 2 Diabetes.Journal of clinical medicine · 2026Article
- Tubular Epithelia-Specific Deletion of MCP-1 Does Not Afford Protection Against Adriamycin-Induced Kidney Injury.International journal of molecular sciences · 2026Article
- The glomerular endothelial glycocalyx as a therapeutic target in proteinuric kidney disease.Nature reviews. Nephrology · 2026Review
- Inflammation and Diabetic Kidney Disease.International journal of molecular sciences · 2026Review
- Capturing the inflammatory landscape within kidney compartments of human diabetic kidney disease: a digital spatial profiling study.Frontiers in endocrinology · 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
- Caloric restriction protects from acute and chronic kidney injury by inhibiting monocyte recruitment.iScience · 2025Article
- Innate immune cells in acute and chronic kidney disease.Nature reviews. Nephrology · 2025Review
- Admission glucose, HbA1c levels and inflammatory cytokines in patients with acute ST-elevation myocardial infarction.Clinical proteomics · 2025Article
- REDD1 expression in podocytes facilitates renal inflammation and pyroptosis in streptozotocin-induced diabetic nephropathy.Cell death & disease · 2025Article
- The Role of Mesenchymal Stem Cells in Treating Diabetic Kidney Disease: Immunomodulatory Effects and Kidney Regeneration.International journal of medical sciences · 2025Article
- The Effect and Mechanism of Fufang Banbianlian Injection in the Treatment of Mesangial Proliferative Glomerulonephritis.Combinatorial chemistry & high throughput screening · 2025Article
- Renal microcirculation and mechanisms in diabetic kidney disease.Frontiers in endocrinology · 2025Review
- Fiery Connections: Macrophage-Mediated Inflammation, the Journey from Obesity to Type 2 Diabetes Mellitus and Diabetic Kidney Disease.Biomedicines · 2024Review
139 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
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy involves a renal inflammatory response induced by the diabetic milieu. Macrophages accumulate in diabetic kidneys in association with the local upregulation of monocyte chemoattractant protein-1 (MCP-1); however, the contribution of macrophages to renal injury and the importance of MCP-1 to their accrual are unclear. Therefore, we examined the progression of streptozotocin (STZ)-induced diabetic nephropathy in mice deficient in MCP-1 in order to explore the role of MCP-1-mediated macrophage accumulation in the development of diabetic kidney damage. Renal pathology was examined at 2, 8, 12 and 18 weeks after STZ treatment in MCP-1 intact (+/+) and deficient (-/-) mice with equivalent blood glucose and hemoglobin A1c levels. In MCP-1(+/+) mice, the development of diabetic nephropathy was associated with increased kidney MCP-1 production, which occurred mostly in tubules, consistent with our in vitro finding that elements of the diabetic milieu (high glucose and advanced glycation end products) directly stimulate tubular MCP-1 secretion. Diabetes of 18 weeks resulted in albuminuria and elevated plasma creatinine in MCP-1(+/+) mice, but these aspects of renal injury were largely suppressed in MCP-1(-/-) mice. Protection from nephropathy in diabetic MCP-1(-/-) mice was associated with marked reductions in glomerular and interstitial macrophage accumulation, histological damage and renal fibrosis. Diabetic MCP-1(-/-) mice also had a smaller proportion of kidney macrophages expressing markers of activation (inducible nitric oxide synthase or sialoadhesin) compared to diabetic MCP-1(+/+) mice. In conclusion, our study demonstrates that MCP-1-mediated macrophage accumulation and activation plays a critical role in the development of STZ-induced mouse diabetic nephropathy.
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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.