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Transforming growth factor- and the progression of renal disease
Author(s) -
Ivonne Loeffler,
Günter Wolf
Publication year - 2013
Publication title -
nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gft267
Subject(s) - medicine , podocyte , glomerulosclerosis , smad , transforming growth factor , renal hypertrophy , extracellular matrix , fibrosis , pathophysiology , signal transduction , transforming growth factor beta , focal segmental glomerulosclerosis , kidney , cancer research , endocrinology , glomerulonephritis , microbiology and biotechnology , diabetic nephropathy , biology , proteinuria
Transforming growth factor-β (TGF-β) is a profibrotic cytokine found in chronic renal diseases, which initiates and modulates a variety of pathophysiological processes. It is synthesized by many renal cell types and exerts its biological functions through a variety of signalling pathways, including the Smad and MAPK pathways. In renal diseases, TGF-β is upregulated and induces renal cells to produce extracellular matrix proteins leading to glomerulosclerosis as well as tubulointerstitial fibrosis. Different types of renal cells undergo different pathophysiological changes induced by TGF-β, leading to apoptosis, hypertrophy and abnormalities of podocyte foot processes, which ultimately result in renal dysfunction. In this review, we describe the effects of TGF-β on different renal cell types and the means by which TGF-β participates in the pathomechanisms of glomerular and tubulointerstitial diseases.

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