ReviewPediatric nephrology (Berlin, Germany)2009
Renin-angiotensin system-growth factor cross-talk: a novel mechanism for ureteric bud morphogenesis.
Review in Pediatric nephrology (Berlin, Germany), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 29 citations in OpenAlex.
- Identification of the regulatory mechanism of ACE2 in COVID-19-induced kidney damage with systems genetics approach.Journal of molecular medicine (Berlin, Germany) · 2023Article
- Local renin-angiotensin systems in the genitourinary tract.Naunyn-Schmiedeberg's archives of pharmacology · 2012Review
- Wnt signaling and renal medulla formation.Pediatric nephrology (Berlin, Germany) · 2011Review
- Activation of skin renin-angiotensin system in diabetic rats.Endocrine · 2011Article
- Genetics of congenital anomalies of the kidney and urinary tract.Pediatric nephrology (Berlin, Germany) · 2011Review
- Receptor tyrosine kinases in kidney development.Journal of signal transduction · 2011Article
- Characterization of mesonephric development and regeneration using transgenic zebrafish.American journal of physiology. Renal physiology · 2010Article
- Cyst formation in the PKD2 (1-703) transgenic rat precedes deregulation of proliferation-related pathways.BMC nephrology · 2010Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
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.
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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.