ArticleThe American journal of pathology2016
Macrophage A2A Adenosine Receptors Are Essential to Protect from Progressive Kidney Injury.
Article in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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.
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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.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Microbiota-associated metabolic networks in gut-kidney communication and renal immune regulation: mechanisms and therapeutic potential.Frontiers in microbiology · 2026Review
- Production of Acetylcholine by Podocytes and its Protection from Kidney Injury in GN.Journal of the American Society of Nephrology : JASN · 2025Article
- Adenosine A2A Receptor Activation Alleviated Disease of Mice with SystemicJournal of inflammation research · 2025Article
- Monocytes and Macrophages in Kidney Disease and Homeostasis.International journal of molecular sciences · 2024Review
- Cathepsin D interacts with adenosine AThe Journal of biological chemistry · 2022Article
- Only Hyperuricemia with Crystalluria, but not Asymptomatic Hyperuricemia, Drives Progression of Chronic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2020Article
- Adenosine ABiomedicines · 2020Article
- [High-salt exposure induces macrophage polarization to promote proliferation and phenotypic transformation of co-cultured renal fibroblasts].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- Extracellular Nucleotides and P2 Receptors in Renal Function.Physiological reviews · 2020Review
- Adenosine and the Cardiovascular System.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2019Review
- The Purinergic System as a Pharmacological Target for the Treatment of Immune-Mediated Inflammatory Diseases.Pharmacological reviews · 2019Review
- Different effects of global osteopontin and macrophage osteopontin in glomerular injury.American journal of physiology. Renal physiology · 2018Article
- P2Y2R Signaling Is Involved in the Onset of Glomerulonephritis.Frontiers in immunology · 2018Article
- Genetic Models of Macrophage Depletion.Methods in molecular biology (Clifton, N.J.) · 2018Review
- Purinergic Signalling: Therapeutic Developments.Frontiers in pharmacology · 2017Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
A2A adenosine receptors (A2ARs) are endogenous inhibitor of inflammation. Macrophages that are key effectors of kidney disease progression express A2ARs. We investigated the role of A2ARs in kidney inflammation in a macrophage-mediated anti-glomerular basement membrane reactive serum-induced immune nephritis in A2AR-deficient mice. Sub-threshold doses of glomerular basement membrane-reactive serum induced more severe and prolonged kidney damage with higher levels of proinflammatory cytokines and greater accumulation of inflammatory cells in A2AR(-/-) mice than wild-type (WT) mice. To investigate the role of macrophage A2AR in progressive kidney injury, glomerulonephritis was induced in CD11b-DTR transgenic mice. Macrophages were selectively depleted in the established phase of the disease and reconstituted with macrophages from WT or A2AR-deficient mice and then treated with an A2AR agonist. In mice receiving WT macrophages and treated with an A2AR agonist, the glomerular cellularity, crescent formation, sclerotic glomeruli, and tubulointerstitial injury were significantly reduced compared with the control group. In contrast, in mice reconstituted with A2AR-deficient macrophages and treated with an A2AR agonist, the kidney injury was more severe with increased deposition of collagen I, III, and IV. These findings suggest that disruption of the protective A2AR amplifies inflammation to accelerate glomerular damage and endogenous macrophage A2ARs are essential to protect from progressive kidney fibrosis.
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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.