Transforming growth factor β (TGFβ) and related molecules in chronic kidney disease (CKD)

The incidence of chronic kidney diseases (CKDs) is expected to rise, fuelled by the ever increasing epidemic of Type 2 diabetes. Despite extensive research in this area, there are currently no effective treatments available to sufficiently halt the progression of CKD towards renal failure. This is largely due to ongoing secondary pathological processes generally elicited by the onset of disease. Fibrosis, in particular, is a prominent pathological hallmark of many forms of CKD and considered to be a central contributing factor for the progression of CKD towards end-stage renal disease. Transforming growth factor beta (TGF beta) has been implicated to be a major regulatory cytokine in CKD, especially in fibrosis development, and reduced TGF beta signalling activity has been previously shown to be associated with improved renal outcomes in experimental animal studies. A number of molecules related to and/or interacting with the TGF beta signalling pathway have been identified as potential therapeutic targets. However, due to its pleiotropic nature, complete inhibition of the TGF beta signalling pathway is likely to lead to deleterious side effects. Therefore, a better understanding of this pathway and the molecules modulating this pathway is necessary to develop more efficacious and therapeutic strategies to combat progression of CKD.