TGF-β in diabetic kidney disease: Role of novel signaling pathways

Kumar Sharma, Tracy A. McGowan

Producción científica: Review articlerevisión exhaustiva

81 Citas (Scopus)


Diabetic nephropathy is the leading cause of end-stage renal disease in the United States and is a major contributing cause of morbidity and mortality in patients with diabetes. Despite conventional therapy to improve glycemic and blood pressure control the incidence of diabetic nephropathy is reaching epidemic proportions worldwide. As the major pathologic feature of diabetic nephropathy is diffuse mesangial matrix expansion, the pro-sclerotic cytokine transforming growth factor-β, TGF-β, is a leading candidate to mediate the progression of the disease. Numerous studies have now demonstrated that TGF-β is a key factor in experimental models of diabetic kidney disease as well as in patients with diabetic nephropathy. Recent studies have begun to explore the mechanisms by which TGF-β is stimulated by high glucose and how TGF-β exerts its matrix-stimulating effects on renal cells. TGF-β may also be involved in mediating the vascular dysfunction of diabetic kidney disease via its effects on the key intracellular calcium channel, the inositol trisphosphate receptor (IP3R). As there is substantial evidence for a cause and effect relationship between upregulation of TGF-β and the progression of diabetic kidney disease, future studies will seek to establish specific targets along these pathways at which to intervene.

Idioma originalEnglish (US)
Páginas (desde-hasta)115-123
Número de páginas9
PublicaciónCytokine and Growth Factor Reviews
EstadoPublished - abr 2000
Publicado de forma externa

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology
  • Endocrinology, Diabetes and Metabolism
  • Immunology and Allergy
  • Immunology


Profundice en los temas de investigación de 'TGF-β in diabetic kidney disease: Role of novel signaling pathways'. En conjunto forman una huella única.

Citar esto