Document Detail

Cell volume regulatory mechanisms in progression of renal disease.
MedLine Citation:
PMID:  11730263     Owner:  NLM     Status:  MEDLINE    
One of the striking morphological features of renal failure is an increase of cell volume. This review explores the role of cell volume regulatory mechanisms in the pathophysiology of progressive renal disease. The case is made that TGF-beta, a major cytokine involved in the development of progressive renal failure, upregulates the transcription of the serum and glucocorticoid-dependent kinase hSGK1, involved in cell volume regulation. Excessive extracellular glucose concentrations stimulate TGF-beta1 expression and thus similarly enhance hSGK1-transcription. The kinase stimulates two mechanisms important for cell volume regulation, i.e. the renal epithelial Na+ channel ENaC and the thick ascending limb Na+,K+,2Cl- cotransporter BSC1. On the one hand, stimulation of renal tubular transport leads to renal retention of Na+, which favours the development of hypertension. On the other, the increase of cell volume stimulates protein synthesis and inhibits protein degradation, contributing to the enhanced net formation and deposition of matrix proteins. At later stages, the increase of cell volume may be reversed to atrophy, and cell death may lead to loss of functional tissue. In conclusion, progressive renal disease is paralleled by deranged cell volume regulatory mechanisms.
S Wärntges; H J Gröne; G Capasso; F Lang
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Journal of nephrology     Volume:  14     ISSN:  1121-8428     ISO Abbreviation:  J. Nephrol.     Publication Date:    2001 Sep-Oct
Date Detail:
Created Date:  2001-12-03     Completed Date:  2002-04-16     Revised Date:  2011-11-02    
Medline Journal Info:
Nlm Unique ID:  9012268     Medline TA:  J Nephrol     Country:  Italy    
Other Details:
Languages:  eng     Pagination:  319-26     Citation Subset:  IM    
Department for Physiology, University of Tübingen, Germany.
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MeSH Terms
Activin Receptors, Type I / biosynthesis*,  genetics
Cell Membrane / metabolism
Cell Size / physiology
Disease Progression
Gene Expression Regulation
Glucose / metabolism
Immediate-Early Proteins
Kidney Diseases / physiopathology*
Kidney Tubules / cytology*,  metabolism
Nuclear Proteins*
Osmolar Concentration
Protein-Serine-Threonine Kinases / biosynthesis,  genetics
Proteins / metabolism
Receptors, Transforming Growth Factor beta / biosynthesis*,  genetics
Signal Transduction
Sodium-Potassium-Chloride Symporters / metabolism*
Reg. No./Substance:
0/Immediate-Early Proteins; 0/Nuclear Proteins; 0/Proteins; 0/Receptors, Transforming Growth Factor beta; 0/Sodium-Potassium-Chloride Symporters; 50-99-7/Glucose; EC type I receptor; EC Kinases; EC regulated kinase; EC Receptors, Type I

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