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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.
One of the causes of renal anemia is the shortened lifespan of red blood cells (RBCs). We previously demonstrated that a decline in flippase activity in the early stage of RBCs leads to increased externalization of phosphatidylserine (PS), contributing to renal anemia. In healthy individuals, flippase ATP11C in senescent RBCs decreases to 62% of that in young RBCs, and it was hypothesized that ATP11C may also be reduced in senescent RBCs of patients with renal anemia. When intracellular Ca²⁺ levels in RBCs were artificially elevated, ATP11C was found to translocate into the microvesicles, which were generated from RBCs' membrane.
To elucidate the mechanism of ATP11C reduction, we conducted proteomic analyses of the membrane cytoskelton protein of young and senescent RBCs from both patients and healthy controls.
Although individual variation was considerable, ATP11C levels in senescent RBCs of renal anemia patients averaged 47% of those in young RBCs, showing a more pronounced decrease compared to healthy controls. Proteomic analysis revealed that in senescent RBCs from renal anemia patients, components of the 4.1R complex—such as Protein 4.1R, Dematin, and Glycophorin C—were decreased relative to healthy controls. In contrast, components of the ankyrin complex, including Ankyrin, Glycophorin A, and Band 3, were preserved.
In addition to the mechanism that increased intracellular Ca²⁺ levels weaken the binding between Protein 4.1R and Glycophorin C, our findings suggest that certain factors associated with renal failure may also weaken the binding between membrane cytoskelton protein and produce microvesicles, leading to a greater reduction of ATP11C.
