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. Author manuscript; available in PMC: 2018 Dec 10.
Published in final edited form as: Nat Rev Nephrol. 2014 Mar 25;10(5):257–267. doi: 10.1038/nrneph.2014.31

Figure 1.

Figure 1

Specific targets and potential therapeutic strategies to inhibit or slow the progression of CKD. There is a complex feed-forward relationship between the initiating factors (hyperglycaemia, obesity, hypertension, bone and mineral disorders) and cardiovascular disorders that stimulate and regulate a variety of major pathways leading to CKD and its complications. Inhibiting intrinsic renal pathways linked to inflammation (NADPH oxidase) and fibrosis (Smads, TGF-β, and CTGF) might prove beneficial. A possible central pathway would be the activation of AMPK that can reduce both inflammatory and profibrotic pathways. Abbreviations: AICAR, AMP analogue; AMPK, 5’-AMP-activated protein kinase; BMP-7, bone morphogenetic protein 7; CKD, chronic kidney disease; CTGF, connective tissue growth factor; EMT, epithelial–mesenchymal transition; HGF, hepatocyte growth factor; NF, nuclear factor; NOX, NADPH oxidase; R, receptor; ROS, reactive oxygen species; Smad, mothers against decapentaplegic homologue; TGF-β, transforming growth factor β; USF, upstream stimulatory factor.