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New insights into the role of podocytes in proteinuria

Disturbances in many different molecular pathways and interactions can lead to the same clinical end points of proteinuria and end-stage renal disease. Proteinuria is often accompanied by a cytopathological change in the glomerulus that is referred to as effacement (retraction) of the podocyte foot... Full description

Journal Title: Nature reviews. Nephrology 2009-08, Vol.5 (8), p.463-468
Main Author: Patrakka, Jaakko
Other Authors: Tryggvason, Karl
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Alma/SFX Local Collection
Publisher: England: Nature Publishing Group
ID: ISSN: 1759-5061
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title: New insights into the role of podocytes in proteinuria
format: Article
creator:
  • Patrakka, Jaakko
  • Tryggvason, Karl
subjects:
  • Adaptor Proteins, Signal Transducing - physiology
  • Animals
  • Endothelium, Vascular - pathology
  • Endothelium, Vascular - physiopathology
  • Genes
  • Genetic aspects
  • Glomerular Basement Membrane - pathology
  • Glomerular Basement Membrane - physiopathology
  • Glomerular Filtration Rate - physiology
  • Humans
  • Kidney diseases
  • Kidney Glomerulus - cytology
  • Kidney Glomerulus - pathology
  • Kidney Glomerulus - physiopathology
  • Medicin och hälsovetenskap
  • Molecular Motor Proteins - genetics
  • Myosin Heavy Chains - genetics
  • Physiological aspects
  • Podocytes - pathology
  • Podocytes - physiology
  • Proteinuria
  • Proteinuria - genetics
  • Proteinuria - pathology
  • Proteinuria - physiopathology
  • Receptor, Notch1 - physiology
  • Receptors, Urokinase Plasminogen Activator - physiology
  • Risk factors
  • TRPC Cation Channels - physiology
  • TRPC6 Cation Channel
  • Type C Phospholipases - genetics
ispartof: Nature reviews. Nephrology, 2009-08, Vol.5 (8), p.463-468
description: Disturbances in many different molecular pathways and interactions can lead to the same clinical end points of proteinuria and end-stage renal disease. Proteinuria is often accompanied by a cytopathological change in the glomerulus that is referred to as effacement (retraction) of the podocyte foot processes. The molecular mechanisms that lead to proteinuria and podocyte effacement are poorly understood; therefore, targeted therapies are lacking. During the past 5 years, however, a large body of data has emerged in this field. The discovery of podocyte gene defects that underlie some hereditary proteinuric syndromes has changed our understanding of the relative contributions of components of the glomerular filter. Furthermore, pathogenic pathways activated in podocytes during proteinuria have been identified. Together, these findings pinpoint the podocyte as the most obvious candidate for therapeutic intervention. In the near future, the use of large-scale expression profiling platforms, transgenic mouse lines, and other in vivo gene delivery methods will further expand our understanding of the pathology of the glomerular filtration barrier, and perhaps reveal novel target molecules for the therapy of proteinuric kidney diseases.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 1759-5061
fulltext: fulltext
issn:
  • 1759-5061
  • 1759-507X
  • 1759-507X
url: Link


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descriptionDisturbances in many different molecular pathways and interactions can lead to the same clinical end points of proteinuria and end-stage renal disease. Proteinuria is often accompanied by a cytopathological change in the glomerulus that is referred to as effacement (retraction) of the podocyte foot processes. The molecular mechanisms that lead to proteinuria and podocyte effacement are poorly understood; therefore, targeted therapies are lacking. During the past 5 years, however, a large body of data has emerged in this field. The discovery of podocyte gene defects that underlie some hereditary proteinuric syndromes has changed our understanding of the relative contributions of components of the glomerular filter. Furthermore, pathogenic pathways activated in podocytes during proteinuria have been identified. Together, these findings pinpoint the podocyte as the most obvious candidate for therapeutic intervention. In the near future, the use of large-scale expression profiling platforms, transgenic mouse lines, and other in vivo gene delivery methods will further expand our understanding of the pathology of the glomerular filtration barrier, and perhaps reveal novel target molecules for the therapy of proteinuric kidney diseases.
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subjectAdaptor Proteins, Signal Transducing - physiology ; Animals ; Endothelium, Vascular - pathology ; Endothelium, Vascular - physiopathology ; Genes ; Genetic aspects ; Glomerular Basement Membrane - pathology ; Glomerular Basement Membrane - physiopathology ; Glomerular Filtration Rate - physiology ; Humans ; Kidney diseases ; Kidney Glomerulus - cytology ; Kidney Glomerulus - pathology ; Kidney Glomerulus - physiopathology ; Medicin och hälsovetenskap ; Molecular Motor Proteins - genetics ; Myosin Heavy Chains - genetics ; Physiological aspects ; Podocytes - pathology ; Podocytes - physiology ; Proteinuria ; Proteinuria - genetics ; Proteinuria - pathology ; Proteinuria - physiopathology ; Receptor, Notch1 - physiology ; Receptors, Urokinase Plasminogen Activator - physiology ; Risk factors ; TRPC Cation Channels - physiology ; TRPC6 Cation Channel ; Type C Phospholipases - genetics
ispartofNature reviews. Nephrology, 2009-08, Vol.5 (8), p.463-468
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descriptionDisturbances in many different molecular pathways and interactions can lead to the same clinical end points of proteinuria and end-stage renal disease. Proteinuria is often accompanied by a cytopathological change in the glomerulus that is referred to as effacement (retraction) of the podocyte foot processes. The molecular mechanisms that lead to proteinuria and podocyte effacement are poorly understood; therefore, targeted therapies are lacking. During the past 5 years, however, a large body of data has emerged in this field. The discovery of podocyte gene defects that underlie some hereditary proteinuric syndromes has changed our understanding of the relative contributions of components of the glomerular filter. Furthermore, pathogenic pathways activated in podocytes during proteinuria have been identified. Together, these findings pinpoint the podocyte as the most obvious candidate for therapeutic intervention. In the near future, the use of large-scale expression profiling platforms, transgenic mouse lines, and other in vivo gene delivery methods will further expand our understanding of the pathology of the glomerular filtration barrier, and perhaps reveal novel target molecules for the therapy of proteinuric kidney diseases.
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6Glomerular Basement Membrane - pathology
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10Kidney diseases
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16Myosin Heavy Chains - genetics
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21Proteinuria - genetics
22Proteinuria - pathology
23Proteinuria - physiopathology
24Receptor, Notch1 - physiology
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abstractDisturbances in many different molecular pathways and interactions can lead to the same clinical end points of proteinuria and end-stage renal disease. Proteinuria is often accompanied by a cytopathological change in the glomerulus that is referred to as effacement (retraction) of the podocyte foot processes. The molecular mechanisms that lead to proteinuria and podocyte effacement are poorly understood; therefore, targeted therapies are lacking. During the past 5 years, however, a large body of data has emerged in this field. The discovery of podocyte gene defects that underlie some hereditary proteinuric syndromes has changed our understanding of the relative contributions of components of the glomerular filter. Furthermore, pathogenic pathways activated in podocytes during proteinuria have been identified. Together, these findings pinpoint the podocyte as the most obvious candidate for therapeutic intervention. In the near future, the use of large-scale expression profiling platforms, transgenic mouse lines, and other in vivo gene delivery methods will further expand our understanding of the pathology of the glomerular filtration barrier, and perhaps reveal novel target molecules for the therapy of proteinuric kidney diseases.
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