Evidence for TGF-β-Mediated ‘Defense’ of the Glomerulus: A Blackguard Molecule Rehabilitated?

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Abstract
Transforming growth factor beta (TGF-β) has been regarded as a ‘blackguard molecule’ that induces glomerular diseases. During the process of glomerulonephritis, upregulated TGF-β stimulates the production of extracellular matrix and inhibits its degradation, leading to excessive matrix deposition. On the other hand, TGF-β 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-β in the glomerulus and to address its ‘bright side’ in glomerular inflammation.