Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
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.
Obesity is a major global health concern and is associated with increased vulnerability to acute kidney injury (AKI). However, the mechanisms by which obesity aggravates sepsis-induced AKI remain unclear. We hypothesized that pre-existing lipid stress in obesity leads to impaired autophagy and renders the kidney more susceptible to mitochondrial injury during sepsis. We further evaluated whether BAM15, a mitochondrial uncoupler, mitigates these pathological processes.
Male C57BL/6J mice were fed either a control diet (CD) or high-fat diet (HFD) for 8 weeks. Cecal ligation and puncture (CLP) was then performed to induce sepsis, with BAM15 administered at the time of CLP in designated groups. Blood and kidneys were collected 6 and 24 h post-CLP. Renal function was assessed by serum creatinine. Transmission electron microscopy (×3000) was used to evaluate mitochondrial morphology, phospholipid accumulation, and autophagy-related organelles in proximal tubular cells.
Sepsis-induced AKI was more severe in obese mice (CD 0.53 ± 0.30 vs. HFD 0.77 ± 0.34 mg/dL, p=0.0148). BAM15 markedly improved renal dysfunction in obese septic mice (HFD-Vehicle 0.72 ± 0.27 vs. HFD-BAM15 0.20 ± 0.08 mg/dL, p<0.0001). Obese mice exhibited baseline phospholipid accumulation, and developed mitochondrial swelling and disrupted cristae architecture after CLP. Autolysosome formation was blunted in obese septic mice, indicating impaired autophagy. BAM15 attenuated mitochondrial injury and partially restored autophagy activity.
Obesity impairs autophagy and predisposes the kidney to mitochondrial injury during sepsis, thereby exacerbating AKI. BAM15 ameliorates this injury, likely by preserving mitochondrial integrity and improving autophagy flux.
