Evidence for TGF-beta-mediated 'defense' of the glomerulus: a blackguard molecule rehabilitated?
Transforming growth factor beta (TGF-beta) has been regarded as a 'blackguard molecule' that induces glomerular diseases. During the process of glomerulonephritis, upregulated TGF-beta stimulates the production of extracellular matrix and inhibits its degradation, leading to excessive matrix deposition. On the other hand, TGF-beta has the potential to be anti-inflammatory via inhibition of mitogenesis and production of inflammatory mediators by glomerular cells. This molecule strongly inactivates infiltrating cells, especially macrophages, which play a pivotal role in the generation of glomerular injury. The aim of this article is to summarize the potentially beneficial action of TGF-beta in the glomerulus and to address its 'bright side' in glomerular inflammation.
Kitamura
M
M
Department of Medicine, University College London Medical School, UK. m.kitamura@medicine.ucl.ac.uk
Fine
L G
LG
D000818:Animals; D017209:Apoptosis; D006801:Humans; D007249:Inflammation / Q000517:prevention & control; D007674:Kidney Diseases / Q000517:prevention & control*; D007678:Kidney Glomerulus; D008264:Macrophages / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000502:physiology*
D016212:Transforming Growth Factor beta