CDA1 enhances the TGF-b/Smad3 signaling pathway by increasing TbRI levels, leading to increased fibrosis. Schematic diagram showing the relationships of CDA1 with profibrotic and anti-inflammatory pathways in the pathogenesis of DKD. In conclusion, there is a large body of experimental data to support the view that targeting CDA1 is a superior approach to directly targeting TGF-ОІ in DKD since it is not only safe but also efficacious in retarding both fibrosis and inflammation. Indeed, targeting CDA1 in experimental DKD not only attenuates diabetes-associated renal fibrosis but also attenuates the expression of key pro-inflammatory genes such as tumor necrosis factor-О± (TNF-О±) and Monocyte Che moattractant Protein-1 (MCP-1). CDA1 has also been found to be an inhibitor of SIRT1 in the DNA damage response. Cell division autoantigen 1 (CDA1) synergistically enhances the profibrotic effect of TGF-ОІ in DKD by regulating the expression of the TGF-ОІ type I receptor (TОІRI). It is postulated that a reduction in renal SIRT1 levels could play a key role in the pathogenesis of DKD and that restoration of SIRT1 will attenuate DKD. Sirtuin-1 (SIRT1) is a protein deacetylase that has been shown to be renoprotective with an anti-inflammatory effect. Among these pathways, the transforming growth factor-ОІ (TGF-ОІ) pathway plays a key pathological role by promoting fibrosis. There are a large number of independent and overlapping profibrotic and pro-inflammatory pathways involved in the pathogenesis and progression of DKD. Renal fibrosis and inflammation are the major pathological features of DKD. DKD is a progressive chronic kidney disease (CKD) and is a leading cause of mortality and morbidity in patients with diabetes. Diabetic kidney disease (DKD) is seen in both type 1 and type 2 diabetes and can be detected in up to 30вЂ“50% of diabetic subjects. Diabetes is a noncommunicable disease and arguably represents the greatest pandemic in human history.

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