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Moreover, the study shows that in vitro over-expressing of -klotho in human proximal tubular cells decreases IGF-1-induced AKT phosphorylation, indicating that the inhibitory effects of -klotho on compensatory renal hypertrophy may be mediated, at least in part, through reduced IGF-1 signaling.28 Notably, inhibition of the GH receptor by the specific antagonism G120K-PEG blocks renal IGF-1 upregulation and subsequent kidney hypertrophy in Uni-Nx animals