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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.
Metabolic stress from high-fat high-sucrose (HFHS) intake induces renal injury by impairing mitochondrial function and promoting lipid peroxidation. Farnesoid X receptor (FXR) is a key regulator of bile acid and lipid metabolism, yet its role in HFHS-induced renal ferroptosis remains unclear. To investigate how FXR deficiency modulates bile acid–lipid remodeling and ferroptotic pathways in HFHS-induced kidney injury.
Male wild-type (WT) and FXR knockout (FXR KO) mice were fed standard chow or an HFHS diet for 5 month. Kidney pathology was assessed by trichrome staining. Plasma bile acids (e.g., LCA, DCA, CDCA, CA, TCA) and lipids (LPC 22:5, LPC 20:5, PE 36:1) were analyzed by targeted metabolomics. Western blotting and immunostaining were used to evaluate GPX4, ACSL4, 4-HNE, and mitochondrial biogenesis markers (PGC‑1α, TFAM).
HFHS-fed WT and FXR KO mice developed renal tubular injury and disrupted bile acid balance, with elevated 12‑OH bile acids (DCA) and non‑12‑OH species (LCA) and non‑12‑OH species (LCA), indicating impaired enterohepatic regulation. Plasma lipidomics revealed a pro-ferroptotic profile characterized by increased LPC 22:5 and PE 36:1, and decreased LPC 20:5. In FXR KO mice, HFHS feeding further impaired bile acid profiles, notably reducing CA, TCA, and CDCA. These alterations were associated with pronounced GPX4 and PGC‑1α downregulation, reduced mitochondrial protective capacity, and increased renal lipid peroxidation (4-HNE, MDA). Together, these results highlight that FXR loss exacerbates HFHS-induced renal injury through bile acid–lysophospholipid–ferroptosis axis dysregulation.
FXR serves as a critical modulator of bile acid–lipid crosstalk in metabolic kidney injury. Its absence sensitizes the kidney to ferroptotic stress under HFHS conditions by amplifying disruptions in both bile acid metabolism and ferroptosis-prone lipid profiles. Therapeutic strategies targeting the FXR–bile acid–lipid axis may offer new avenues to mitigate diet-induced ferroptosis and renal dysfunction.
