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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Statins have been suggested to exert antifibrotic effects in kidney disease, but their preventive potential remains unclear. Therefore, we aimed to investigate whether statin pretreatment can attenuate kidney fibrosis in a bilateral ischemia-reperfusion injury (bIRIx) model.
Mice were pretreated with atorvastatin (10 mg/kg/day) or vehicle for three days before bIRIx, and kidneys were collected three days later for fibrosis marker analysis. To investigate underlying mechanisms, MDCK cells were transfected with HOXA13-specific siRNA, treated with atorvastatin, and stimulated with TGF-β1 (5 ng/mL), followed by assessment of fibrosis markers.
Mice subjected to bIRIx developed significant severe tubulointerstitial fibrosis, as evidenced by elevated expression of TGF-β1 (2.5 ± 0.2 vs. control, p<0.001), collagen (2.8 ± 0.2 vs. control, p<0.001), and monocyte chemoattractant protein-1 (MCP-1; 3.3 ± 0.1 vs. control, p<0.001), along with marked collagen deposition, α-smooth muscle actin (α-SMA) expression, and F4/80-positive macrophage infiltration. Atorvastatin pretreatment significantly attenuated kidney fibrosis and inflammation, reducing TGF-β1 (2.5 ± 0.2 vs.1.7 ± 0.1, p<0.01), collagen (2.8 ± 0.2 vs. 1.8 ± 0.1, p<0.001), MCP-1 (3.3 ± 0.1 vs. 2.0 ± 0.1, p<0.001) compared to bIRIx alone. In vitro, atorvastatin attenuated TGF-β1-induced upregulation of collagen (2.9 ± 0.2 vs. 6.8 ± 0.3, p<0.001), α-SMA (2.3 ± 0.2 vs. 5.0 ± 0.3, p<0.001), and USAG-1 (3.4 ± 0.4 vs. 7.4 ± 0.4, p<0.001). Importantly, HOXA13 knockdown abolished the inhibitory effect of atorvastatin on USAG-1 (3.4 ± 0.4 vs.5.6 ± 0.2, p<0.001) and reversed its antifibrotic effects on collagen (2.9 ± 0.2 vs. 4.9 ± 0.1, p<0.001) and α-SMA (2.3 ± 0.2 vs. 3.8 ± 0.1, p<0.001), suggesting a critical role for HOXA13 in mediating these responses.
Our results suggest that atorvastatin pretreatment prevents kidney fibrosis, partly by regulating HOXA13, USAG-1, and BMP-7. These findings indicate atorvastatin may have therapeutic potential to prevent kidney fibrosis by modulating profibrotic pathways.
