ArticleTranslational pediatrics2026
TGF-β1 induces epithelial-mesenchymal transition and fibrosis of ureteral epithelial cells via targeting RACK1 in ureteropelvic junction obstruction.
Article in Translational pediatrics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Ureteropelvic junction obstruction (UPJO) is a frequent cause of congenital hydronephrosis. It involves both structural and functional changes at the ureteropelvic junction (UPJ), where the ureter connects with the renal pelvis. The mechanisms behind tissue remodeling and fibrosis in this condition are not fully understood. This study explores the role of epithelial-mesenchymal transition (EMT) and examines how receptor for activated C kinase 1 (RACK1) may regulate this process in UPJO. Methods: Stenotic UPJ tissues were collected from patients with congenital UPJO and analyzed for EMT and RACK1 expression. An Results: EMT features, including increased expression of N-cadherin, β-catenin, Vimentin, and ECM-related proteins (COL1A1, FN1, α-SMA), and decreased E-cadherin expression, were observed in both UPJO tissues and TGF-β1-treated cells. RACK1 was significantly upregulated in stenotic tissues and after TGF-β1 stimulation. RACK1 knockdown suppressed Smad2/3 and p65 activation, inhibited EMT features, and reduced cell proliferation and migration. Conclusions: EMT features are associated with tissue remodeling and fibrosis in congenital UPJO. RACK1 promotes TGF-β1-induced EMT through activation of Smad2/3 and p65 signaling. These findings provide new insights into the pathogenesis of UPJO and suggest RACK1 as a potential target for therapeutic intervention.
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