RESEARCH ARTICLE


TGF-β Made Easy



N. Garcia-Fernandez , M.L. Marco Molina*
Clínica Universitaria de Navarra, Departments of Nephrology and General Surgery, Pio XII 38, Pamplona 31008, Pamplona, Navarra, Spain


Article Metrics

CrossRef Citations:
1
Total Statistics:

Full-Text HTML Views: 4117
Abstract HTML Views: 2239
PDF Downloads: 807
ePub Downloads: 730
Total Views/Downloads: 7893
Unique Statistics:

Full-Text HTML Views: 1480
Abstract HTML Views: 1118
PDF Downloads: 505
ePub Downloads: 462
Total Views/Downloads: 3565



Creative Commons License
2008 Bentham Science Publishers Ltd.

* Address correspondence to this author at the Clínica Universitaria de Navarra, Departments of Nephrology and General Surgery, Pio XII 38, Pamplona 31008, Pamplona, Navarra, Spain; Tel: 0034 948255400; E-mail: mmarcomolina@gmail.com


Abstract

Renal fibrosis is the final common pathway of several nephropathies including chronic allograft failure. Most chronic renal diseases result in tissue fibrosis, and this is independent of their initial cause. Tissue fibrosis is an accumulation of extracellular matrix, and in animal models of renal fibrosis, mRNA levels for profibrogenic cytokines such as transforming growth factor β (TGFβ) and extracellular matrix (ECM) molecular components are up regulated and they precede glomerulosclerosis and interstitial fibrosis. TGFβ 1 plays a crucial role in renal fibrosis. In this review the main features of this important cytokine and existing previous therapeutic attempts to inhibit TGFβ expression are briefly summarised.