ReviewFrontiers in immunology2026
Calcimimetics and CaSR signaling in CKD-MBD: bone-immune-vascular crosstalk and therapeutic potential.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
Chronic kidney disease (CKD) disrupts mineral metabolism, skeletal remodeling, vascular homeostasis, and immune regulation, producing the systemic phenotype of CKD-mineral and bone disorder (CKD-MBD) together with chronic inflammation and impaired host defense. Osteoimmunology provides a framework for understanding how bone cells, immune cells, and vascular cells interact through shared mediators such as RANKL, osteoprotegerin, NF-kappaB, NFATc1, inflammatory cytokines, fibroblast growth factor 23 (FGF23), Wnt inhibitors, and phosphate-dependent osteogenic signaling pathways. The calcium-sensing receptor (CaSR) is a class C G protein-coupled receptor that regulates parathyroid hormone (PTH) secretion and can signal through Gαq/11, Gαi/o, Gα12/13, and beta-arrestin-dependent pathways. CaSR expression and/or calcium-sensing responses have been described in bone cells, selected immune-lineage cells, and vascular smooth muscle cells, suggesting that CaSR may participate in bone-immune-vascular communication. Calcimimetics, including cinacalcet, etelcalcetide, and evocalcet, are established CaSR-targeting therapies for secondary hyperparathyroidism in dialysis patients. Their best-validated actions are PTH suppression and improvement of calcium-phosphate biochemical control; clinical and experimental studies also support reductions in FGF23, selected bone-turnover markers, and vascular calcification measures. This review critically evaluates the pharmacology of calcimimetics and their potential osteoimmune relevance in CKD-MBD. We emphasize established clinical effects while distinguishing them from mechanistic hypotheses, including direct NLRP3 inflammasome suppression, Th17/Treg rebalancing, macrophage M1-to-M2 polarization, osteocyte connexin-43/DAMP regulation, and hematopoietic niche restoration, which remain insufficiently validated in human CKD. We propose an integrated bone-vascular-immune framework and identify biomarker-guided and precision-medicine strategies for future calcimimetic research.
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