ArticleScientific reports2018
(Pro)renin receptor is involved in mesangial fibrosis and matrix expansion.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 29 citations in OpenAlex.
- Indoxyl sulfate in the gut-kidney axis: from diet-microbiome interactions to renal injury and targeted therapies.Frontiers in nutrition · 2026Review
- Potential of soluble (pro)renin receptor in kidney disease: can it go beyond a biomarker?American journal of physiology. Renal physiology · 2022Review
- Sex differences in soluble prorenin receptor in patients with type 2 diabetes.Biology of sex differences · 2021Article
- (Pro)renin receptor in the kidney: function and significance.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Review
- Serum-soluble (pro)renin receptor concentration as a biomarker for organ damage in primary aldosteronism.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Article
- The (pro)renin receptor in health and disease.Nature reviews. Nephrology · 2019Review
- Suppression of Choroidal Neovascularization and Fibrosis by a Novel RNAi Therapeutic Agent against (Pro)renin Receptor.Molecular therapy. Nucleic acids · 2019Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
(Pro)renin receptor [(P)RR] is expressed in the kidney and is involved in renal injury. Although (P)RR is activated by indoxyl sulfate (IS) and may be related to renal injury, the details remain unclear. We used mouse mesangial cell line SV40 MES13 to investigate the association of (P)RR with mesangial fibrosis or expansion. Furthermore, we examined the correlation between serum soluble (P)RR [s(P)RR] and various laboratory data including serum IS, a uremic toxin that induces renal fibrosis through (P)RR, and pathological indices in chronic kidney disease and particularly in IgA nephropathy patients. In vitro study using SV40 MES13 cells revealed that (P)RR expression significantly increased in the presence of IS. IS stimulated the fibrotic factors' expression, which was significantly suppressed by (P)RR knockdown. Moreover, it significantly increased the expression of matrix metalloproteinase 9 and tissue inhibitor of metalloproteinase 1 via the ERK1/2 pathway. In addition, the s(P)RR level significantly correlated with serum IS and mesangial injury markers in our patients. Our results suggest that (P)RR is associated with mesangial fibrosis and matrix expansion through the IS-(P)RR-ERK1/2 pathway. Clinically, s(P)RR may be a biomarker of mesangial fibrosis and matrix expansion.
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Registered trials
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