Cited by 322Renin-Angiotensin System StudiesChronic Kidney Disease and DiabetesRenal and Vascular Pathologies

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Succinate receptor GPR91 provides a direct link between high glucose levels and renin release in murine and rabbit kidney

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Toma, Ildikó, Kang, Jung Julie, Sipos, Arnold, Vargas, Sarah, Bansal, Eric, Hanner, Fiona, Meer, Elliott, Peti-Peterdi, János·2008·Journal of Clinical Investigation

DOI 10.1172/jci33293PMC PMC2413183

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Abstract

Diabetes mellitus is the most common and rapidly growing cause of end-stage renal disease in developed countries. A classic hallmark of early diabetes mellitus includes activation of the renin-angiotensin system (RAS), which may lead to hypertension and renal tissue injury, but the mechanism of RAS activation is elusive. Here we identified a paracrine signaling pathway in the kidney in which high levels of glucose directly triggered the release of the prohypertensive hormone renin. The signaling cascade involved the local accumulation of succinate and activation of the kidney-specific G protein-coupled metabolic receptor, GPR91, in the glomerular endothelium as observed in rat, mouse, and rabbit kidney sections. Elements of signal transduction included endothelial Ca2+, the production of NO and prostaglandin (PGE2), and their paracrine actions on adjacent renin-producing cells. This GPR91 signaling cascade may serve to modulate kidney function and help remove metabolic waste products through renal hyperfiltration, and it could also link metabolic diseases, such as diabetes, or metabolic syndrome with RAS overactivation, systemic hypertension, and organ injury.

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Authors: Toma, I., Kang, J. J., Sipos, A., Vargas, S., Bansal, E., Hanner, F., Meer, E., & Peti-Peterdi, J.
Affiliations: University of Southern California (US)
ORCID: Kang, Jung Julie
Sipos, Arnold
Vargas, Sarah
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2008-06-01
Volume: 118
Issue: 7
Pages: 2526-34
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci33293
PMC: PMC2413183
OpenAlex: W2125951881
Cited by: 322
References: 47
Citations by year: 2026: 5 · 2025: 16 · 2024: 19 · 2023: 17 · 2022: 21 · 2021: 26 · 2020: 24 · 2019: 23 · 2018: 17 · 2017: 21 · 2016: 16 · 2015: 11 · 2014: 12 · 2013: 22 · 2012: 16
FWCI: 12.90
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute of Diabetes and Digestive and Kidney Diseases (DK 64324, DK37097, DK 74754, R01DK074754, R01DK037097, R01DK064324)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
Health Sciences › Medicine › Nephrology › Renal and Vascular Pathologies
Keywords: GPR91, succinate receptor, renin secretion, high glucose, renin-angiotensin system, diabetes mellitus, kidney, glomerular endothelium, paracrine signaling, nitric oxide, prostaglandin E2, calcium signaling, hypertension, renal hyperfiltration, metabolic syndrome, end-stage renal disease
MeSH terms: Animals, Citrates, Diabetes Mellitus, Experimental, Female, Glucose, Hyperglycemia, Juxtaglomerular Apparatus, Kidney, Male, Malonates, Mice, Inbred C57BL, Mice, Transgenic, Nitric Oxide, Rabbits, Renin, Dinoprostone, Mice, Knockout, Succinic Acid, Paracrine Communication, Calcium Signaling, Endothelial Cells, Receptors, G-Protein-Coupled, Mice, Rats

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Succinate receptor GPR91 provides a direct link between high glucose levels and renin release in murine and rabbit kidney

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