The transforming growth factor beta system in kidney disease and repair: Recent progress and future directions

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Abstract

Transforming growth factor beta is a multifunctional polypeptide growth factor implicated in a variety of renal diseases. The expression of transforming growth factor beta is enhanced in renal diseases and available evidence suggests that its activity in promoting the synthesis of extracellular matrix plays a crucial role in fibrotic deposition and the decline in renal function. Transforming growth factor beta is, however, also expressed in response to renal injury and may play an important role in normal repair processes. It appears that renal diseases may result from the inappropriate regulation of transforming growth factor beta expression. The determination of the factors that mediate transforming growth factor beta activity will be of primary importance in elucidating the mechanisms leading to renal disease or repair after injury. Both in-vitro and in-vivo studies have demonstrated that proteolytic activity, thrombospondin-1, elevated glucose, angiotensin II, oxidant stress and hemodynamic forces regulate transforming growth factor beta activity through both transcriptional and post-transcriptional mechanisms. In some cases, therapies that may partly disrupt renal transforming growth factor beta activity have shown promise in slowing the progression to end-stage renal disease.

Original languageEnglish (US)
Pages (from-to)21-30
Number of pages10
JournalCurrent Opinion in Nephrology and Hypertension
Volume8
Issue number1
DOIs
StatePublished - 1999
Externally publishedYes

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Kidney Diseases
Transforming Growth Factor beta
Kidney
Thrombospondin 1
Wounds and Injuries
Direction compound
Oxidants
Angiotensin II
Chronic Kidney Failure
Extracellular Matrix
Intercellular Signaling Peptides and Proteins
Hemodynamics
Glucose
Peptides

ASJC Scopus subject areas

  • Nephrology
  • Internal Medicine

Cite this

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abstract = "Transforming growth factor beta is a multifunctional polypeptide growth factor implicated in a variety of renal diseases. The expression of transforming growth factor beta is enhanced in renal diseases and available evidence suggests that its activity in promoting the synthesis of extracellular matrix plays a crucial role in fibrotic deposition and the decline in renal function. Transforming growth factor beta is, however, also expressed in response to renal injury and may play an important role in normal repair processes. It appears that renal diseases may result from the inappropriate regulation of transforming growth factor beta expression. The determination of the factors that mediate transforming growth factor beta activity will be of primary importance in elucidating the mechanisms leading to renal disease or repair after injury. Both in-vitro and in-vivo studies have demonstrated that proteolytic activity, thrombospondin-1, elevated glucose, angiotensin II, oxidant stress and hemodynamic forces regulate transforming growth factor beta activity through both transcriptional and post-transcriptional mechanisms. In some cases, therapies that may partly disrupt renal transforming growth factor beta activity have shown promise in slowing the progression to end-stage renal disease.",
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