ArticleJournal of the American Society of Nephrology : JASN2008
Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.
Article in Journal of the American Society of Nephrology : JASN, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 87 citations in OpenAlex.
- Specificity of endothelial cells in endothelial dysfunction of diabetic kidney disease and their crosstalk with neighboring cells: an updated review.Frontiers in endocrinology · 2025Review
- Adenosine receptors as emerging therapeutic targets for diabetic kidney disease.Kidney research and clinical practice · 2022Article
- Role of the macula densa sodium glucose cotransporter type 1-neuronal nitric oxide synthase-tubuloglomerular feedback pathway in diabetic hyperfiltration.Kidney international · 2022Article
- Update on Pathogenesis of Glomerular Hyperfiltration in Early Diabetic Kidney Disease.Frontiers in endocrinology · 2022Review
- Knockout of Macula Densa Neuronal Nitric Oxide Synthase Increases Blood Pressure in db/db Mice.Hypertension (Dallas, Tex. : 1979) · 2021Article
- A New Hope in Type 2 Diabetes Mellitus Management: Sodium-Glucose Cotransporter 2 Inhibitors.Cureus · 2021Review
- Relevance of the Pyroptosis-Related Inflammasome Pathway in the Pathogenesis of Diabetic Kidney Disease.Frontiers in immunology · 2021Review
- Adenosine A1 Receptor Deficiency Aggravates Extracellular Matrix Accumulation in Diabetic Nephropathy through Disturbance of Peritubular Microenvironment.Journal of diabetes research · 2021Article
- Adenosine ABiomedicines · 2020Article
- A role for tubular NaAmerican journal of physiology. Renal physiology · 2020Article
- Tubular effects of sodium-glucose cotransporter 2 inhibitors: intended and unintended consequences.Current opinion in nephrology and hypertension · 2020Review
- The tubular hypothesis of nephron filtration and diabetic kidney disease.Nature reviews. Nephrology · 2020Review
- Article
- Alteration of purinergic signaling in diabetes: Focus on vascular function.Journal of molecular and cellular cardiology · 2020Review
- Podocyte Density and Albuminuria in Aging Diabetic Ins2± Mice with or Without Adenosine A1 Receptor Signaling.International journal of nephrology and renovascular disease · 2020Article
- The effect of A1 adenosine receptor in diabetic megalin loss with caspase-1/IL18 signaling.Diabetes, metabolic syndrome and obesity : targets and therapy · 2019Article
- Diabetes downregulates renal adenosine A2A receptors in an experimental model of hypertension.PloS one · 2019Article
- Sodium glucose cotransporter 2 in mesangial cells and retinal pericytes and its implications for diabetic nephropathy and retinopathy.Glycobiology · 2017Article
- Sodium-Glucose Cotransporter 2 Inhibitors with Renoprotective Effects.Kidney diseases (Basel, Switzerland) · 2017Review
- SGLT2 Protein Expression Is Increased in Human Diabetic Nephropathy: SGLT2 PROTEIN INHIBITION DECREASES RENAL LIPID ACCUMULATION, INFLAMMATION, AND THE DEVELOPMENT OF NEPHROPATHY IN DIABETIC MICE.The Journal of biological chemistry · 2017Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Intraglomerular hypertension and glomerular hyperfiltration likely contribute to the pathogenesis of diabetic nephropathy, and tubuloglomerular feedback (TGF) has been suggested to play a role in diabetic hyperfiltration. A1 adenosine receptor (A1AR) null mice lack a TGF response, so this model was used to investigate the contribution of TGF to hyperfiltration in diabetic Ins2(+/-) Akita mice. TGF responses in Ins2(+/-) A1AR(-/-) double mutants were abolished, whereas they were attenuated in Ins2(+/-) mice. GFR, assessed at 14, 24, and 33 wk, was approximately 30% higher in Ins2(+/-) than in wild-type (WT) mice and increased further in Ins2(+/-) A1AR(-/-) mutants (P < 0.01 versus both WT and Ins2(+/-) mice at all ages). Histologic evidence of glomerular injury and urinary albumin excretion were more pronounced in double-mutant than single-mutant or WT mice. In summary, the marked elevation of GFR in diabetic mice that lack a TGF response indicates that TGF is not required to cause hyperfiltration in the Akita model of diabetes. Rather, an A1AR-dependent mechanism, possibly TGF, limits the degree of diabetic hyperfiltration and nephropathy.
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