Down-regulation of Smad7 expression by ubiquitin-dependent degradation contributes to renal fibrosis in obstructive nephropathy in mice.

@article{Fukasawa2004DownregulationOS,
  title={Down-regulation of Smad7 expression by ubiquitin-dependent degradation contributes to renal fibrosis in obstructive nephropathy in mice.},
  author={Hirotaka Fukasawa and Tatsuo Yamamoto and Akashi Togawa and Naro Ohashi and Yoshihide Fujigaki and Toshiaki Oda and Chiharu Uchida and Kyoko Kitagawa and Takayuki Hattori and Sayuri Suzuki and Masatoshi Kitagawa and Akira Hishida},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={2004},
  volume={101 23},
  pages={8687-92}
}
Overexpression of transforming growth factor beta (TGF-beta) has been shown to play pathogenic roles in progression of renal fibrosis, and the severity of tubulointerstitial fibrosis correlates better with renal function than the severity of glomerulosclerosis. Smad proteins are signaling transducers downstream from TGF-beta receptors. Three families of Smad proteins have been identified: receptor-regulated Smad2 and Smad3, common partner Smad4, and inhibitory Smad7 (part of a negative-feedback… CONTINUE READING