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Titolo:
Cell volume regulatory mechanisms in progression of renal disease
Autore:
Warntges, S; Grone, HJ; Capasso, G; Lang, F;
Indirizzi:
Univ Tubingen, Dept Physiol, Tubingen, Germany Univ Tubingen Tubingen Germany ubingen, Dept Physiol, Tubingen, Germany
Titolo Testata:
JOURNAL OF NEPHROLOGY
fascicolo: 5, volume: 14, anno: 2001,
pagine: 319 - 326
SICI:
1121-8428(200109/10)14:5<319:CVRMIP>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; GROWTH-FACTOR-BETA; GLOMERULAR MESANGIAL CELLS; TGF-BETA; GENE-EXPRESSION; TUBULOINTERSTITIAL INJURY; DIABETIC NEPHROPATHY; ALDOSE REDUCTASE; XENOPUS OOCYTES; H-SGK;
Keywords:
TGF-beta 1; matrix proteins; glucose; intracellular Ca++ activity; hSGK; cell volume regulation; diabetic nephropathy; epithelial Na+ channel; Na+,K+,2Cl(-) cotransporter;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
125
Recensione:
Indirizzi per estratti:
Indirizzo: Lang, F Univ Tubingen, Inst Physiol, Gmelinstr 5, D-76072 Tubingen, Germany Univ Tubingen Gmelinstr 5 Tubingen Germany D-76072 ingen, Germany
Citazione:
S. Warntges et al., "Cell volume regulatory mechanisms in progression of renal disease", J NEPHROL, 14(5), 2001, pp. 319-326

Abstract

One of the striking morphological features of renal failure is an increaseof 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, theincrease 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.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/04/20 alle ore 02:06:44