Fig. 8: A model of NEDD4-2-dependent control of kidney disease progression. | Cell Death & Disease

Fig. 8: A model of NEDD4-2-dependent control of kidney disease progression.

From: The ubiquitin ligase NEDD4-2/NEDD4L regulates both sodium homeostasis and fibrotic signaling to prevent end-stage renal disease

Fig. 8

NEDD4-2 regulates several molecular processes that contribute to the progression of kidney disease, including Na+ transport and fibrotic signaling pathways. This occurs through ubiquitination of substrates such as ENaC (and other channels and transporters) as well as downstream components of Wnt/β-catenin/TGF-β1 signaling pathways. In the absence of NEDD4-2, increased Na+ contributes to sustained tubular damage with a mild reduction in kidney function. Sustained signaling through Wnt and TGF-β1 pathways, particularly as a result of high dietary Na+, drives increased kidney damage and severely decreased renal function suggesting progression from CKD to ESRD. Figure created with BioRender.com.

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