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A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
Published on: October 26, 2020
(Pro)renin Receptor in Kidney Development and Disease
1Section of Pediatric Nephrology, Department of Pediatrics, Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, 1430 Tulane Avenue, New Orleans, LA 70112, USA.
Abstract:
The renin-angiotensin system (RAS), a key regulator of the blood pressure and fluid/electrolyte homeostasis, also plays a critical role in kidney development. All the components of the RAS are expressed in the developing metanephros. Moreover, mutations in the genes encoding components of the RAS in mice or humans are associated with a broad spectrum of congenital anomalies of the kidney and urinary tract (CAKUT). These forms of CAKUT include renal papillary hypoplasia, hydronephrosis, duplicated collecting system, renal tubular dysgenesis, renal vascular abnormalities, and aberrant glomerulogenesis. Emerging evidence indicates that (pro)renin receptor (PRR), a novel component of the RAS, is essential for proper kidney development and that aberrant PRR signaling is causally linked to cardiovascular and renal disease. This paper describes the role of the RAS in kidney development and highlights emerging insights into the cellular and molecular mechanisms by which the PRR may regulate this critical morphogenetic process.
Insights
The renin-angiotensin system (RAS) is crucial for kidney development, with its components expressed in the developing kidney. Aberrant RAS signaling, including the novel (pro)renin receptor (PRR), is linked to congenital kidney anomalies.
Area of Science:
- Nephrology
- Developmental Biology
- Endocrinology
Background:
- The renin-angiotensin system (RAS) regulates blood pressure and fluid balance.
- RAS components are present in the developing kidney (metanephros).
- Mutations in RAS genes cause congenital anomalies of the kidney and urinary tract (CAKUT).
Purpose of the Study:
- To describe the role of the RAS in kidney development.
- To highlight the function of the (pro)renin receptor (PRR) in kidney morphogenesis.
- To explore PRR signaling in cardiovascular and renal disease.
Main Methods:
- Review of existing literature on RAS and kidney development.
- Analysis of genetic studies linking RAS components to CAKUT.
- Examination of emerging evidence on PRR function.
Main Results:
- RAS is essential for normal kidney development.
- Defects in RAS components lead to various CAKUT.
- The (pro)renin receptor (PRR) is vital for kidney development.
- Aberrant PRR signaling is associated with renal and cardiovascular diseases.
Conclusions:
- The RAS plays a fundamental role in kidney development.
- PRR is a key regulator of kidney morphogenesis.
- Understanding PRR mechanisms may offer therapeutic targets for kidney diseases.
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