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Updated: Jun 28, 2026

Dissection and Culture of Mouse Embryonic Kidney
Published on: May 17, 2017
Renin-angiotensin system-growth factor cross-talk: a novel mechanism for ureteric bud morphogenesis
1Section of Pediatric Nephrology, Department of Pediatrics, Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, LA, USA. iiosipi@tulane.edu
Abstract:
The renin-angiotensin system (RAS) plays a critical role in kidney development. Mutations in the genes encoding components of the RAS cause a spectrum of congenital abnormalities of the kidney and renal collecting system, ranging from hypoplasia of the renal medulla and hydronephrosis in mice to renal tubular dysgenesis in humans. However, the mechanisms by which an intact RAS controls proper renal system development and how aberrations in the RAS result in abnormal kidney and renal collecting system development are poorly understood. The renal collecting system originates from the ureteric bud (UB). A number of transcription and growth factors regulate UB branching morphogenesis to ultimately form the ureter, pelvis, calyces, medullary, and cortical collecting ducts. Importantly, UB morphogenesis is a key developmental process that controls organogenesis of the entire metanephros. This review emphasizes emerging insights into the role for the RAS in UB morphogenesis and explores the mechanisms whereby RAS regulates this important process. A conceptual framework derived from recent work indicates that cooperation between the angiotensin II AT(1) receptor and receptor tyrosine kinase signaling performs essential functions during renal collecting system development via control of UB branching morphogenesis.
Insights
The renin-angiotensin system (RAS) is crucial for kidney development. This review explores how RAS controls ureteric bud branching morphogenesis, essential for forming a healthy renal collecting system.
Area of Science:
- Developmental Biology
- Renal Physiology
- Molecular Biology
Background:
- The renin-angiotensin system (RAS) is vital for kidney development.
- RAS gene mutations lead to congenital kidney and renal collecting system abnormalities.
- Mechanisms of RAS control over renal development are not fully understood.
Purpose of the Study:
- To review the role of the RAS in ureteric bud (UB) morphogenesis.
- To explore mechanisms by which RAS regulates UB branching.
- To provide a framework for understanding RAS in renal development.
Main Methods:
- Literature review focusing on RAS and kidney development.
- Analysis of genetic and molecular pathways involved in UB morphogenesis.
- Integration of findings on receptor tyrosine kinase and AT(1) receptor signaling.
Main Results:
- The RAS plays a critical role in regulating ureteric bud branching morphogenesis.
- Aberrations in RAS signaling pathways result in abnormal kidney development.
- Cooperation between angiotensin II AT(1) receptor and receptor tyrosine kinase signaling is essential.
Conclusions:
- The RAS is a key regulator of renal collecting system development via UB branching.
- Understanding RAS mechanisms offers insights into congenital kidney diseases.
- Targeting RAS pathways may hold potential for therapeutic interventions.
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