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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.
Salt-sensitive hypertension develops following ischemia–reperfusion injury (IRI) in rats, with distal nephron sodium transporters playing a key role in the pathogenesis. We investigated the effects of peroxisome proliferator-activated receptor alpha (PPARα) activation by pemafibrate on IRI-induced salt-sensitive hypertension and hypertensive renal injury.
Sprague-Dawley rats underwent right nephrectomy, followed 14 days later by transient left renal artery clamping to induce IRI. Rats were then provided 1.0% NaCl in drinking water (IRI/NaCl) to promote salt-sensitive hypertension. Pemafibrate (0.3 mg/kg), a selective PPARα modulator, was administered via chow beginning 2 weeks prior to IRI induction. Blood pressure, renal histology, molecular markers, and immune cell subsets were evaluated.
Pemafibrate upregulated PPARα expression in kidney tissue and significantly reduced blood pressure in IRI/NaCl rats. The expression of phosphorylated NCC, a sodium transporter in the distal nephron, was notably suppressed. Pemafibrate also reduced tubular injury and renal fibrosis, as evidenced by decreased fibrotic area on histology. Immunohistochemistry revealed attenuated deposition of α-SMA and collagen I, and reduced infiltration of CD68⁺ macrophages. Western blot analysis showed inhibition of NLRP3 inflammasome activation, caspase-1 cleavage, and IL-1β expression in pemafibrate-treated rats. Flow cytometry analysis further demonstrated a significant increase in CD86⁺CD163⁺ macrophage subsets in the pemafibrate group, suggesting an immunomodulatory shift toward a mixed activation phenotype. Additionally, gene expression analysis revealed downregulation of inflammatory and fibrotic mediators, while nuclear translocation of PPARα was enhanced in tubular epithelial cells, consistent with transcriptional activation.
Pemafibrate, a selective PPARα modulator, ameliorates salt-sensitive hypertension and hypertensive kidney injury after IRI in rats by suppressing NLRP3-mediated inflammation, inhibiting NCC activation, and promoting CD86⁺CD163⁺ macrophage expansion. These findings suggest pemafibrate as a potential therapeutic agent for salt-sensitive hypertension and its associated organ damage.
