Transforming Growth Factor-Beta and the Kidney: What We Know and What We Can Do?

Transforming growth factor-β (TGF-β) and its receptors are expressed in the kidney. The effects of TGF-β are mainly through activation of Smad pathways. In different pathophysiological situations such as development, immunomodulation, fibrosis and cell response, TGF-β interacts with other factors including angiotensin II, plasminogen activator inhibitor-1, connective tissue growth factor, integrins, and thymosin β4. Clinical studies have shown that specific polymorphisms of TGF-β genes and increased serum, urine and biopsied specimen levels are associated with human renal diseases. However, the effects of inhibition of TGF-β system are complex, depending on the injury type, disease stage and dosage of the inhibitor. Several animal studies have shown beneficial effects anti-TGF-β especially in chronic renal diseases, while data from clinical studies are still limited. In this review, current knowledge about the role of TGF-β system in the kidney and potential of strategies to modulate TGF-β for renoprotection are discussed.