Cell and Molecular Biology of Kidney Development

Kimberly J. Reidy, Norman D. Rosenblum

Research output: Contribution to journalArticle

96 Citations (Scopus)

Abstract

Abnormalities of kidney and urinary tract development are the most common cause of end-stage kidney failure in childhood in the United States. Over the past 20 years, the advent of mutant and transgenic mice and the manipulation of gene expression in other animal models has resulted in major advances in identification of the cellular and molecular mechanisms that direct kidney morphogenesis, providing insights into the pathophysiology of renal and urologic anomalies. This review focuses on the molecular mechanisms that define kidney progenitor cell populations, induce nephron formation within the metanephric mesenchyme, initiate and organize ureteric bud branching, and participate in terminal differentiation of the nephron. Highlighted are common signaling pathways that function at multiple stages during kidney development, including signaling via Wnts, bone morphogenic proteins, fibroblast growth factor, sonic hedgehog, RET/glial cell-derived neurotrophic factor, and notch pathways. Also emphasized are the roles of transcription factors Odd1, Eya1, Pax2, Lim1, and WT-1 in directing renal development. Areas requiring future investigation include the factors that modulate signaling pathways to provide temporal and site-specific effects. The evolution of our understanding of the cellular and molecular mechanisms of kidney development may provide methods for improved diagnosis of renal anomalies and, hopefully, targets for intervention for this common cause of childhood end-stage kidney disease.

Original languageEnglish (US)
Pages (from-to)321-337
Number of pages17
JournalSeminars in Nephrology
Volume29
Issue number4
DOIs
StatePublished - Jul 2009

Fingerprint

Cell Biology
Molecular Biology
Kidney
Nephrons
Hedgehogs
Fibroblast Growth Factors
Nerve Growth Factors
Mesoderm
Urinary Tract
Morphogenesis
Neuroglia
Transgenic Mice
Chronic Kidney Failure
Renal Insufficiency
Transcription Factors
Stem Cells
Animal Models
Gene Expression
Bone and Bones
Population

Keywords

  • differentiation
  • Genes
  • kidney development
  • metanephric mesenchyme
  • nephron
  • progenitor
  • ureteric bud

ASJC Scopus subject areas

  • Nephrology

Cite this

Cell and Molecular Biology of Kidney Development. / Reidy, Kimberly J.; Rosenblum, Norman D.

In: Seminars in Nephrology, Vol. 29, No. 4, 07.2009, p. 321-337.

Research output: Contribution to journalArticle

Reidy, Kimberly J. ; Rosenblum, Norman D. / Cell and Molecular Biology of Kidney Development. In: Seminars in Nephrology. 2009 ; Vol. 29, No. 4. pp. 321-337.
@article{e5d74fb8466a42d69abbc9208d01f23c,
title = "Cell and Molecular Biology of Kidney Development",
abstract = "Abnormalities of kidney and urinary tract development are the most common cause of end-stage kidney failure in childhood in the United States. Over the past 20 years, the advent of mutant and transgenic mice and the manipulation of gene expression in other animal models has resulted in major advances in identification of the cellular and molecular mechanisms that direct kidney morphogenesis, providing insights into the pathophysiology of renal and urologic anomalies. This review focuses on the molecular mechanisms that define kidney progenitor cell populations, induce nephron formation within the metanephric mesenchyme, initiate and organize ureteric bud branching, and participate in terminal differentiation of the nephron. Highlighted are common signaling pathways that function at multiple stages during kidney development, including signaling via Wnts, bone morphogenic proteins, fibroblast growth factor, sonic hedgehog, RET/glial cell-derived neurotrophic factor, and notch pathways. Also emphasized are the roles of transcription factors Odd1, Eya1, Pax2, Lim1, and WT-1 in directing renal development. Areas requiring future investigation include the factors that modulate signaling pathways to provide temporal and site-specific effects. The evolution of our understanding of the cellular and molecular mechanisms of kidney development may provide methods for improved diagnosis of renal anomalies and, hopefully, targets for intervention for this common cause of childhood end-stage kidney disease.",
keywords = "differentiation, Genes, kidney development, metanephric mesenchyme, nephron, progenitor, ureteric bud",
author = "Reidy, {Kimberly J.} and Rosenblum, {Norman D.}",
year = "2009",
month = "7",
doi = "10.1016/j.semnephrol.2009.03.009",
language = "English (US)",
volume = "29",
pages = "321--337",
journal = "Seminars in Nephrology",
issn = "0270-9295",
publisher = "W.B. Saunders Ltd",
number = "4",

}

TY - JOUR

T1 - Cell and Molecular Biology of Kidney Development

AU - Reidy, Kimberly J.

AU - Rosenblum, Norman D.

PY - 2009/7

Y1 - 2009/7

N2 - Abnormalities of kidney and urinary tract development are the most common cause of end-stage kidney failure in childhood in the United States. Over the past 20 years, the advent of mutant and transgenic mice and the manipulation of gene expression in other animal models has resulted in major advances in identification of the cellular and molecular mechanisms that direct kidney morphogenesis, providing insights into the pathophysiology of renal and urologic anomalies. This review focuses on the molecular mechanisms that define kidney progenitor cell populations, induce nephron formation within the metanephric mesenchyme, initiate and organize ureteric bud branching, and participate in terminal differentiation of the nephron. Highlighted are common signaling pathways that function at multiple stages during kidney development, including signaling via Wnts, bone morphogenic proteins, fibroblast growth factor, sonic hedgehog, RET/glial cell-derived neurotrophic factor, and notch pathways. Also emphasized are the roles of transcription factors Odd1, Eya1, Pax2, Lim1, and WT-1 in directing renal development. Areas requiring future investigation include the factors that modulate signaling pathways to provide temporal and site-specific effects. The evolution of our understanding of the cellular and molecular mechanisms of kidney development may provide methods for improved diagnosis of renal anomalies and, hopefully, targets for intervention for this common cause of childhood end-stage kidney disease.

AB - Abnormalities of kidney and urinary tract development are the most common cause of end-stage kidney failure in childhood in the United States. Over the past 20 years, the advent of mutant and transgenic mice and the manipulation of gene expression in other animal models has resulted in major advances in identification of the cellular and molecular mechanisms that direct kidney morphogenesis, providing insights into the pathophysiology of renal and urologic anomalies. This review focuses on the molecular mechanisms that define kidney progenitor cell populations, induce nephron formation within the metanephric mesenchyme, initiate and organize ureteric bud branching, and participate in terminal differentiation of the nephron. Highlighted are common signaling pathways that function at multiple stages during kidney development, including signaling via Wnts, bone morphogenic proteins, fibroblast growth factor, sonic hedgehog, RET/glial cell-derived neurotrophic factor, and notch pathways. Also emphasized are the roles of transcription factors Odd1, Eya1, Pax2, Lim1, and WT-1 in directing renal development. Areas requiring future investigation include the factors that modulate signaling pathways to provide temporal and site-specific effects. The evolution of our understanding of the cellular and molecular mechanisms of kidney development may provide methods for improved diagnosis of renal anomalies and, hopefully, targets for intervention for this common cause of childhood end-stage kidney disease.

KW - differentiation

KW - Genes

KW - kidney development

KW - metanephric mesenchyme

KW - nephron

KW - progenitor

KW - ureteric bud

UR - http://www.scopus.com/inward/record.url?scp=67650444682&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=67650444682&partnerID=8YFLogxK

U2 - 10.1016/j.semnephrol.2009.03.009

DO - 10.1016/j.semnephrol.2009.03.009

M3 - Article

C2 - 19615554

AN - SCOPUS:67650444682

VL - 29

SP - 321

EP - 337

JO - Seminars in Nephrology

JF - Seminars in Nephrology

SN - 0270-9295

IS - 4

ER -