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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.
Pathological deposition of calcium-phosphate in the arterial wall leads to vascular calcification, which is an important risk factor for cardiovascular mortality in CKD patients. Higher dietary Mg2+ intake was shown to reduce vascular calcification and cardiovascular mortality in clinical studies; however, the mechanisms of Mg2+ effect remain unclear. Extracellular Ca2+-sensing receptor (CaSR) is a protein expressed in many tissues including vascular smooth muscle cells (VSMC). Cyclic adenosine monophosphate (cAMP) is a secondary messenger which is known to drive osteoblastic differentiation and calcification in VSMC. We recently showed that extracellular calcium-sensing receptor (CaSR) is a regulator of the cAMP pathway in intestinal epithelial cells where Mg2+ is the major CaSR agonist. We hypothesized that CaSR activation in VSMC is a major mechanism for the protective effects of Mg2+ in vascular calcification.
The effects of Mg2+ and roles of CaSR were studied in cell and animal models of vascular calcification including a murine CKD model.
In mouse primary aortic smooth muscle cells, calcium-phosphate treatment (3 mM Ca2+, 2.5 mM PO43- for 7 days) resulted in marked calcification. Increasing Mg2+ in culture media concentration-dependently reduced calcification by up to 90% at 1 mM. The protective effects of Mg2+ were essentially abolished by CaSR inhibitor NPS-2143. Mg2+ treatment had minimal effects on calcification in primary cells derived from VSMC-specific CaSR knockout mice (SM22-Cre; Casr-flox), confirming key roles of CaSR in its efficacy. CaSR activation assays showed that Mg2+ is a more potent CaSR agonist than Ca2+ in VSMC at physiological concentrations seen in plasma. Mg2+ effect in VMSC was mediated by reduced cAMP levels, and decreased CREB (cAMP response element binding protein) phosphorylation and RUNX2 (osteoblastic differentiation marker) expression. In a high dose vitamin D-induced vascular calcification model, mice fed with a low (0.02%) Mg2+ diet had severe aortic calcification which was reduced by 32% and 66% in mice fed with normal (0.2%) and high (0.5%) Mg2+ diets, respectively. In an adenine-induced CKD model, increasing dietary Mg2+ reduced vascular calcification severity by >90 % in wild-type mice with minimal effect in VSMC-specific CaSR knockout animals. Higher Mg2+ intake in CKD model increased serum Mg2+ levels without any changes in serum Ca2+, Pi or BUN. In mouse aorta, vascular calcification reduced CaSR expression by 60%, and high Mg2+ diet administration resulted in preserved CaSR expression. Lastly, physiological Mg2+ concentrations reduced calcification severity by >70% in a primary human aortic VSMC model in a CaSR dependent manner.
Our results suggest that Mg2+ reduces vascular calcification by activating CaSR and preventing osteoblastic differentiation in VSMC via reducing cAMP levels. Mg2+ supplementation can be a simple and safe treatment for preventing vascular calcification in CKD.
