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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.
Chronic kidney disease (CKD) often leads to vascular calcification (VC), a severe complication recognized as a major cardiovascular risk factor. The molecular mechanisms underlying CKD-associated VC remain unclear. This study investigates the role of kidney-derived extracellular vesicles (EVs) in mediating CKD-related VC through the transport of complement component C3.
A CKD-VC mouse model was established using adenine combined with a high-phosphate diet. VC was assessed via VonKossa staining in CKD-VC mice treated with GW4869 (an exosome inhibitor), renal EVs, or C3aR inhibitor. Tubular EV trafficking was visualized in vascular walls using immunofluorescence in Tubular EV-tracing mice(Slc34a1 Cre/+;CD63-PAGFP fl/+ mice). Complement activation and localization in renal tubules were evaluated in CKD-VC mice via Western blot (WB), PCR, and immunofluorescence. EVs isolated from renal tissues and plasma were analyzed for C3 and tubular markers by WB. Plasma C3 levels in EVs, EV-depleted plasma, and total plasma were quantified via ELISA. Single-molecule imaging(ONI) and nanoflow cytometry determined the C3 distribution in renal and plasma EVs. Tubular-specific C3 knockdown mice was achieved using adeno-associated virus (AAV) to assess VC. In vitro, vascular smooth muscle cells (VSMCs) treated with high-phosphate were treated with tubular EVs or the C3aR inhibitor SB290157, and then osteogenic differentiation markers, C3aR, and pathway proteins were analyzed by PCR and WB, with calcification visualized via Alizarin Red staining. Plasma EVs from 30 CKD patients with VC and healthy controls were assayed for C3.
Renal EVs exacerbated VC in CKD mice, while GW4869 attenuated calcification. Proteomics revealed high C3 expression in renal EVs. CKD-VC mice exhibited tubular complement activation and EV-mediated C3 secretion into circulation. Plasma EVs from CKD patients showed significantly elevated C3 levels compared to controls. Immunofluorescence confirmed uptake of tubular EVs by calcified vascular walls. In vitro, tubular EVs enhanced VSMC osteogenic differentiation and upregulated C3aR, mimicking C3a effects, while C3aR inhibition reversed these outcomes. Tubular C3 knockdown in vivo reduced VC severity. Clinically, plasma EV C3 levels correlated positively with abdominal aortic calcification scores in CKD-VC patients.
This study demonstrates that tubule-derived EVs mediate vascular smooth muscle osteogenic transdifferentiation and CKD-related VC via C3 transport. Targeting EV-C3 signaling may represent a novel therapeutic strategy for CKD-associated vascular calcification.
