ArticleAmerican journal of physiology. Renal physiology2025
Renal tubular (pro)renin receptor deletion exacerbates kidney injury in
Deborah Stuart, Caitlin S Peterson, Dhruvan Gopinath, Divya Sundar, Will Wheatley, Nirupama Ramkumar
Abstract read
In one paragraphArticle in American journal of physiology. Renal physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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4 · The recordCorrections and comments
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5 · Who and what moneyAuthors and funding
6 authors.
Deborah StuartDivision of Nephrology and Hypertension, Department of Internal Medicine, University of Utah Health, Salt Lake City, Utah, United States.
Caitlin S PetersonDivision of Nephrology and Hypertension, Department of Internal Medicine, University of Utah Health, Salt Lake City, Utah, United States.
Dhruvan GopinathDivision of Nephrology and Hypertension, Department of Internal Medicine, University of Utah Health, Salt Lake City, Utah, United States.
Divya SundarDivision of Nephrology and Hypertension, Department of Internal Medicine, University of Utah Health, Salt Lake City, Utah, United States.
Will WheatleyDivision of Nephrology and Hypertension, Department of Internal Medicine, University of Utah Health, Salt Lake City, Utah, United States.
Nirupama RamkumarDivision of Nephrology and Hypertension, Department of Internal Medicine, University of Utah Health, Salt Lake City, Utah, United States.ORCID 0000-0002-5312-1100 Funding
Soluble (pro)renin receptor regulation of kidney fibrosisR01DK133271 · NIDDK · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI NIRUPAMA RAMKUMAR · 2023 to 2026
$1.8MRole of the soluble (pro)renin receptor in blood pressure regulationR56HL155345 · NHLBI · UNIVERSITY OF UTAH · PI RAMKUMAR, NIRUPAMA · 2021 to 2021
$408kAmerican Diabetes Association (ADA) Junior faculty development grantHHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL155345HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases (DEM) DK133271NHLBI NIH HHS R56 HL155345NIDDK NIH HHS R01 DK133271
6 · The paper itselfAbstract
The (pro)renin receptor (PRR) is a multifunctional protein implicated in blood pressure regulation and kidney fibrosis. Previous studies report enhanced PRR expression in nondiabetic and diabetic kidney disease. In this study, we investigated whether deletion of renal tubular PRR attenuates kidney injury in type 2 diabetes. Floxed PRR mice were bred with mice expressing Pax8 rtTA and LC1 transgenes and
Indexed as
Diabetes Mellitus, Type 2Diabetic NephropathiesKidney TubulesReceptors, Cell SurfaceVacuolar Proton-Translocating ATPasesAlbuminuriaAnimalsBlood GlucoseDisease Models, AnimalMaleMiceMice, Inbred C57BLMice, KnockoutProrenin ReceptorATP6AP2 protein, mouseBlood GlucoseProrenin ReceptorReceptors, Cell SurfaceVacuolar Proton-Translocating ATPasesdiabeteskidney disease(pro)renin receptor
Identifiers
PMID41087039
PMCPMC12643321
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