Therapeutic potential of TGF-β inhibition in chronic renal failure

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.

Keywords::

• progressive nephropathies
• proteinuria
• renal fibrosis
• transforming growth factor-β

Notes

Ac-SDKP: N-Acetyl-seryl-aspartyl-lysyl-proline; ACE: Angiotensin-converting enzyme; BMP: Bone morphogenic protein; HGF: Hepatocyte growth factor; PPAR: Peroxisome proliferator-activated receptor; TGF: Transforming growth factor.