TGF-beta and glomerulonephritis: anti-inflammatory versus prosclerotic actions

Abstract

TGF-beta has been considered as the key regulator in the generation of glomerulosclerosis. Despite abundant descriptive data, it still remains undetermined whether sustained, local expression of TGF-beta leads to irreversible glomerulosclerosis. There is no doubt that TGF-beta stimulates ECM production in the glomerulus, but this molecule has several anti-inflammatory properties as well. Towards a better understanding of the pathogenesis of glomerulonephritis and for the development of novel and efficient therapeutic interventions, extensive efforts should be made to clarify the 'bright side' of TGF-beta as well as its 'dark side' in individual experimental and human diseases, focusing especially on the concentration and the time-point at which its anti-inflammatory properties spill over into its prosclerotic actions.