ArticleScientific reports2026
Rosuvastatin attenuates tubulointerstitial fibrosis by targeting the HOXA13 USAG1 BMP7 pathway.
Article in Scientific reports, 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
Statins act as antifibrotic agents but their mechanism is unclear. Therefore, we aimed to evaluate the antifibrotic effects of rosuvastatin in a chronic kidney fibrosis model in vivo and transforming growth factor-β1 (TGF-β1)-stimulated Madin-Darby canine kidney (MDCK) cells in vitro. Mice with unilateral ischemic reperfusion injury and contralateral nephrectomy (uIRIx) were administered vehicle or rosuvastatin (10 mg/kg/day by oral gavage) for four weeks and kidney fibrosis markers were analyzed. Moreover, control and homeobox protein Hox-A13 (HOXA13) knocked-down MDCK cells were stimulated with TGF-β1 (5 ng/ml) and then treated with rosuvastatin. The uIRIx mice developed severe tubulointerstitial fibrosis with increased α-smooth muscle actin (α-SMA), collagen I and uterine sensitization-associated gene-1 (USAG-1) expression, but rosuvastatin therapy attenuated these expression and improved fibrosis. Rosuvastatin also reduced Smad3 phosphorylation and increased Smad1/5/9 phosphorylation, both associated with bone morphogenetic protein-7 (BMP-7) signaling. TGF-β1-stimulated MDCK cells exhibited increased α-SMA, fibronectin, vimentin, and collagen 1 expression, which rosuvastatin reversed. In addition, TGF-β1-stimulated MDCK cells demonstrated increased USAG-1 expression without changes in BMP-7 expression. Gene knockdown using HOXA13 siRNA suggested rosuvastatin decreased USAG-1 expression by increasing HOXA13 expression. Our results demonstrate that rosuvastatin inhibits kidney fibrosis by activating BMP-7 signaling via upregulation of HOXA13 and downregulation of USAG-1.
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