Transforming Growth Factor-β in Renal Disease

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Abstract

An extensive number of animal and clinical studies indicate that transforming growth factors-β (TGF-βs) play an important role in inflammatory and fibrotic diseases, including renal fibrosis. Recent mouse models harboring genetically engineered alterations in TGF-β pathways reveal complicated mechanisms of regulation of TGF-β activity in vivo. The purpose of this review is to present recent advances relevant to our understanding of the TGF-β-signaling system in renal physiology and pathophysiology.

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Most cited references 19

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Transforming growth factor beta in tissue fibrosis.

W Border, N Noble (1994)

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Targeted disruption of the mouse transforming growth factor-beta 1 gene results in multifocal inflammatory disease.

M Shull, I Ormsby, A Kier … (1992)

Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional growth factor that has profound regulatory effects on many developmental and physiological processes. Disruption of the TGF-beta 1 gene by homologous recombination in murine embryonic stem cells enables mice to be generated that carry the disrupted allele. Animals homozygous for the mutated TGF-beta 1 allele show no gross developmental abnormalities, but about 20 days after birth they succumb to a wasting syndrome accompanied by a multifocal, mixed inflammatory cell response and tissue necrosis, leading to organ failure and death. TGF-beta 1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions.

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Abnormal lung development and cleft palate in mice lacking TGF-beta 3 indicates defects of epithelial-mesenchymal interaction.

V Kaartinen, J W Voncken, C. Shuler … (1995)

A broad spectrum of biological activities has been proposed for transforming growth factor-beta 3 (TGF-beta 3). To study TGF-beta 3 function in development, TGF-beta 3 null mutant mice were generated by gene-targeting. Within 20 hours of birth, homozygous TGF-beta 3-/- mice die with unique and consistent phenotypic features including delayed pulmonary development and defective palatogenesis. Unlike other null mutants with cleft palate, TGF-beta 3-/- mice lack other concomitant craniofacial abnormalities. This study demonstrates an essential function for TGF-beta 3 in the normal morphogenesis of palate and lung, and directly implicates this cytokine in mechanisms of epithelial-mesenchymal interaction.