Key result
(Pro)renin receptor (PRR) promotes kidney injury and fibrosis by amplifying Wnt/β-catenin signaling, acting as both a downstream target and a crucial element in Wnt signal transmission.
Why the study?
Does modulation of the (pro)renin receptor affect Wnt/β-catenin signaling and subsequent kidney injury and fibrosis in CKD models?
Population
Mouse models of CKD, human CKD kidney biopsy specimens, and in vitro cell models
Comparison
Modulation ofrenin receptor expression and… vs Control conditions
Design
Preclinical
Authors
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PRR mediates Wnt/β-catenin signaling in murine CKD models; leaves open human therapeutic targeting.
Does modulation of the (pro)renin receptor affect Wnt/β-catenin signaling and subsequent kidney injury and fibrosis in CKD models?
The (pro)renin receptor promotes kidney injury and fibrosis by amplifying Wnt/β-catenin signaling, highlighting a novel mechanism in CKD pathogenesis.
Li et al. (2017) studied Kidney injury and fibrosis (CKD). (Pro)renin receptor (PRR) modulation vs. Control was evaluated on Kidney dysfunction, inflammation, and fibrotic lesions. (Pro)renin receptor (PRR) promotes kidney injury and fibrosis by amplifying Wnt/β-catenin signaling, acting as both a downstream target and a crucial element in Wnt signal transmission.
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