ArticleJournal of diabetes research2016
Renal Protection by Genetic Deletion of the Atypical Chemokine Receptor ACKR2 in Diabetic OVE Mice.
Article in Journal of diabetes research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Research Progress on Pathogenesis of Diabetic Nephropathy and Intervention with Traditional Chinese Medicine.Journal of multidisciplinary healthcare · 2026Review
- Phosphoproteomic mapping of CCR5 and ACKR2 signaling properties.Frontiers in molecular biosciences · 2022Article
- CD45 Immunohistochemistry in Mouse Kidney.Bio-protocol · 2021Article
- The kidney, COVID-19, and the chemokine network: an intriguing trio.International urology and nephrology · 2021Review
- The Role of Chemokines and Chemokine Receptors in Diabetic Nephropathy.International journal of molecular sciences · 2020Review
- Clopidogrel Reduces Fibronectin Accumulation and Improves Diabetes-Induced Renal Fibrosis.International journal of biological sciences · 2019Article
- Article
- Serotonin and Its Receptor as a New Antioxidant Therapeutic Target for Diabetic Kidney Disease.Journal of diabetes research · 2017Review
- Cytokine decoy and scavenger receptors as key regulators of immunity and inflammation.Cytokine · 2016Article
- Atypical Chemokine Receptors and Their Roles in the Resolution of the Inflammatory Response.Frontiers in immunology · 2016Review
- Roles of pattern recognition receptors in diabetic nephropathy.Journal of Zhejiang University. Science. BReview
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In diabetic nephropathy (DN) proinflammatory chemokines and leukocyte infiltration correlate with tubulointerstitial injury and declining renal function. The atypical chemokine receptor ACKR2 is a chemokine scavenger receptor which binds and sequesters many inflammatory CC chemokines but does not transduce typical G-protein mediated signaling events. ACKR2 is known to regulate diverse inflammatory diseases but its role in DN has not been tested. In this study, we utilized ACKR2(-/-) mice to test whether ACKR2 elimination alters progression of diabetic kidney disease. Elimination of ACKR2 greatly reduced DN in OVE26 mice, an established DN model. Albuminuria was significantly lower at 2, 4, and 6 months of age. ACKR2 deletion did not affect diabetic blood glucose levels but significantly decreased parameters of renal inflammation including leukocyte infiltration and fibrosis. Activation of pathways that increase inflammatory gene expression was attenuated. Human biopsies stained with ACKR2 antibody revealed increased staining in diabetic kidney, especially in some tubule and interstitial cells. The results demonstrate a significant interaction between diabetes and ACKR2 protein in the kidney. Unexpectedly, ACKR2 deletion reduced renal inflammation in diabetes and the ultimate response was a high degree of protection from diabetic nephropathy.
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