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TGF-β signal transduction and mesangial cell fibrogenesis

American Journal of Physiology-Renal Physiology · 2003 · Vol. 284(2) · pp. F243–F252
H. William SchnaperTomoko HayashidaSusan C. HubchakAnne-Christine Poncelet

Abstract

Transforming growth factor-beta (TGF-beta) is closely associated with progressive renal fibrosis. Significant progress has been accomplished in determining the cellular signaling pathways that are activated by TGF-beta. This knowledge is being applied to glomerular mesangial cell models of extracellular matrix (ECM) accumulation. A central component of TGF-beta-stimulated mesangial cell fibrogenesis is the TGF-beta family-specific Smad signal transduction pathway. However, while Smads play an important role in collagen accumulation, recent findings indicate that cross talk among a variety of pathways is necessary for maximal stimulation of collagen expression. Further investigation of these multiple interactions will provide insight into possible ways to interrupt cellular mechanisms of glomerular fibrogenesis.

TGF-β signaling in diseasesChronic Kidney Disease and DiabetesConnective Tissue Growth Factor ResearchSMADExtracellular matrixSignal transductionMesangial cellCell biologyTransforming growth factor betaTransforming growth factorTGF beta signaling pathwayFibrosisBiology

MeSH terms

AnimalsFibrosisGlomerular MesangiumGlomerulosclerosis, Focal SegmentalHumansSignal TransductionTransforming Growth Factor beta
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References
Nephron adaptation to renal injury or ablation
American Journal of Physiology-Renal Physiology · 1985 · 639 citations
Controlling TGF-β signaling
Genes & Development · 2000 · 1,563 citations
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