Abstract
Chronic kidney diseases are emerging as a worldwide public health problem. The progression of kidney diseases closely correlates with the accumulation of extracellular matrix leading to glomerulosclerosis and tubulointerstitial injury. Transforming growth factor (TGF)-β has been identified as a key mediator of kidney matrix accumulation. Overexpression of TGF-β isoforms and their receptors was observed in a variety of renal diseases in both animals and humans. Given its crucial role in fibrotic kidney disease, TGF-β has been recently considered as a possible target in the management of chronic renal diseases. This review discusses the role of TGF-β in renal fibrosis and provides an overview of the strategies that, when interfering with TGF-β expression and signalling, could be employed as new renoprotective treatments.
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