ArticlePloS one2018
(Pro)Renin receptor mediates obesity-induced antinatriuresis and elevated blood pressure via upregulation of the renal epithelial sodium channel.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Nonlinear association of a composite metabolic index (ZJU index) with hypertension: a cross-sectional study of NHANES 2003-2018.Frontiers in cardiovascular medicine · 2025Article
- Nephron specific ATP6AP2 knockout increases urinary excretion of fatty acids and decreases renal cortical megalin expression.Scientific reports · 2024Article
- The (pro)renin receptor as a pharmacological target in cardiorenal diseaes.Hypertension research : official journal of the Japanese Society of Hypertension · 2023Review
- The Epithelial Sodium Channel-An Underestimated Drug Target.International journal of molecular sciences · 2023Review
- Soluble (Pro)Renin Receptor in Hypertension.Nephron · 2023Review
- The role of (pro)renin receptor and its soluble form in cardiovascular diseases.Frontiers in cardiovascular medicine · 2023Review
- Potential of soluble (pro)renin receptor in kidney disease: can it go beyond a biomarker?American journal of physiology. Renal physiology · 2022Review
- Decreased tubuloglomerular feedback response in high-fat diet-induced obesity.American journal of physiology. Renal physiology · 2022Article
- Knockout of Nephron ATP6AP2 Impairs Proximal Tubule Function and Prevents High-Fat Diet-Induced Obesity in Male Mice.Endocrinology · 2021Article
- Soluble (Pro)Renin Receptor as a Negative Regulator of NCC (NaHypertension (Dallas, Tex. : 1979) · 2021Article
- Novel regulation of renal gluconeogenesis by Atp6ap2 in response to high fat diet via PGC1-α/AKT-1 pathway.Scientific reports · 2021Article
- The Pathological Role of Pro(Renin) Receptor in Renal Inflammation.Journal of experimental pharmacology · 2021Review
- Soluble (pro)renin receptor regulation of ENaC involved in aldosterone signaling in cultured collecting duct cells.American journal of physiology. Renal physiology · 2020Article
- Detrimental Effect of C-Reactive Protein on the Cardiometabolic Cells and Its Rectifying by Metabolic Surgery in Obese Diabetic Patients.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
- Low Nitric Oxide Bioavailability Increases Renin Production in the Collecting Duct.Frontiers in physiology · 2020Article
- The (pro)renin receptor: an emerging player in hypertension and metabolic syndrome.Kidney international · 2019Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Recent studies have demonstrated that the renal (pro)renin receptor (PRR) regulates expression of the alpha subunit of the epithelial sodium channel (α-ENaC). In this study we hypothesized that the renal PRR mediates high fat diet (HFD)-induced sodium retention and elevated systolic blood pressure (SBP) by enhancing expression of the epithelial sodium channel (α-ENaC). In our study we used a recently developed inducible nephron specific PRR knockout mouse. Mice (n = 6 each group) were allocated to receive regular diet (RD, 12 kcal% fat) or a high-fat diet (HFD, 45 kcal% fat) for 10 weeks. Body weight (BW), SBP, urine volume (UV) and urine sodium (UNaV), as well as renal interstitial Angiotensin II (Ang II), and renal medullary expression of PRR, p-SGK-1, α-ENaC were monitored in RD and HFD mice with or without PRR knockout. At baseline, there were no significant differences in BW, BP, UV or UNaV between different animal groups. At the end of the study, HFD mice had significant increases in SBP, BW, and significant reductions in UV and UNaV. Compared to RD, HFD significantly increased mRNA and protein expression of PRR, α-ENaC, p-SGK-1, and Ang II. Compared to HFD alone, PRR knockout mice on HFD had reduced mRNA and protein expression of PRR, p-SGK-1, and α-ENaC, as well as increased UV, UNaV and significantly reduced SBP. RIF Ang II was significantly increased by HFD and did not change in response to PRR knockout. We conclude that obesity induced sodium retention and elevated SBP are mediated by the PRR-SGK-1- α-ENaC pathway independent of Ang II.
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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.