Calprotectin Accelerates Pathogenic Calciprotein Particle Maturation to Promote Vascular Calcification in Chronic Kidney Disease.

Myeloid-specific deletion of calprotectin (CPT) in CKD-mineral and bone disorder mice significantly attenuates aortic calcification and osteogenic signaling while shifting circulating CPPs toward an immature fraction.

• Why it matters: Vascular calcification in CKD-mineral and bone disorder is a key driver of cardiovascular mortality, yet how secondary calciprotein particles (CPP2) mature into pathogenic forms is not fully understood.
• What they did: The study used CKD-mineral and bone disorder mice with myeloid-specific CPT deletion, assessed aortic calcification by ex vivo imaging, histology, and calcium quantification, and measured serum CPP fractions by flow cytometry; mechanistic work tested macrophage-derived CPT with CPP2 in vascular smooth muscle cells using T50 and compositional microscopy.
• The result: Macrophage-derived CPT enhanced CPP2-induced smooth muscle calcification by accelerating maturation (shortened T50) and enriching CPP2 in calcium and phosphate, and CPP2 from CPT-deficient serum showed reduced calcification potency, implying CPT shapes particle quality via a TLR4-independent, cell-free milieu.

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