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.
Apolipoprotein M (ApoM) is a carrier of sphingosine-1-phosphate (S1P) and ApoM-S1P exerts potent physiological effects mainly through S1P1 receptor. We previously reported protective effects of ApoM in a multiple organ failure in sepsis mouse model, IgA nephropathy mouse model, and diabetic nephropathy mouse model and its potential as a therapeutic target. Here, we investigated the roles of ApoM in cisplatin-induced nephropathy using a mouse model and potential novel downstream mechanisms modulated by ApoM.
ApoM-knockout mice (KO) and wild-type (WT) mice on a C57BL/6 background received a single intraperitoneal injection of cisplatin (15 or 30 mg/kg). Blood samples were collected, and the mice were euthanized at 96 hours after infection, and their kidneys were harvested for analysis. Plasma creatinine (Cr) was measured. Renal histology was assessed by Periodic acid–Schiff (PAS) staining, and tubular injury area was quantified. Expression of apoptosis-related proteins (Bax, Bcl-2, Bcl-xl, cleaved caspase-3), survival signaling molecules (Akt, SIRT1), mitochondolial biogenesis markers (PGC-1α, and TFAM, ND-1) were analyzed by Western blot. HK-2 cells were used for mechanistic insight, and siRNA mediated knockdown of ApoM was performed.
Cr was elevated in KO mice at both doses: 1.60 mg/dL vs. 2.87 mg/dL (p < 0.01) at 15 mg/kg, and 1.64 mg/dL vs. 5.67 mg/dL (p < 0.01) at 30 mg/kg. Renal histology showed no difference in tubular injury area between WT and KO mice at a dose of 15 mg/kg (13.5% [KO] vs 7.8% [WT], p = 0.23), but KO mice showed severe damage at 30mg/kg (78.2% [KO] vs 9.1% [WT], p = 0.02). Western blot revealed increased cleaved caspase-3 and Bax/Bcl-2 ratios with reduced Akt phosphorylation and SIRT1 expression in KO mice, suggesting enhanced apoptosis. Mitochondrial regulators (PGC-1α, TFAM) were also down-regulated in KO mice, indicating decreased mitochondrial function and metabolic downregulation in injured tubular cells. In HK-2 cells, knockdown of ApoM recapitulated the increased susceptibility to cisplatin.
ApoM knockout mice exhibited worsened renal function in blood tests and histology, along with progressive mitochondrial dysfunction and apoptosis. These findings highlighted ApoM as a critical modulator of renal protection against cisplatin injury and suggested the therapeutic potential of targeting the ApoM/S1P axis in acute kidney injury induced by cisplatin as well as chronic kidney diseases.
