Abstract
Chronic tubulointerstitial damage with tubular epithelial atrophy and interstitial fibrosis is the hallmark of chronic kidney disease (CKD) and a predictor for progression of CKD. Several experiments have now provided evidence that the Wnt signaling pathways are significantly contributing to atrophy and fibrosis;in contrast, it also has been shown that the Wnt system fosters regenerative processes in acute tubular injury. We now have demonstrated that Dickkopf 3 (DKK3) is an agonist for canonical Wnt signaling in CKD and fosters chronic fibrosing inflammation of the tubulointerstitial compartment. Genetic- and antibody-mediated inhibition of DKK3 leads to a pronounced improvement of tubular differentiation and a reduction in fibrosis. In addition, the secreted glycoprotein DKK3 can be used as a non-invasive urinary marker for the extent of CKD in man.
Item Type: | Journal article |
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Faculties: | Medicine |
Subjects: | 600 Technology > 610 Medicine and health |
ISSN: | 0031-6768 |
Language: | English |
Item ID: | 52813 |
Date Deposited: | 14. Jun 2018, 09:51 |
Last Modified: | 04. Nov 2020, 13:31 |