Vascular calcification or ectopic mineralization in blood vessels is an active, cell-regulated process, increasingly recognized as a general cardiovascular risk factor. Remarkably, ectopic artery mineralization is frequently accompanied by decreased bone mineral density or disturbed bone turnover. This contradictory association, observed mainly in osteoporosis and chronic kidney disease, is called the 'calcification paradox'. Here, we review recent advances in our understanding of the calcification paradox, including protein expression patterns governing both normal and ectopic mineralization, the conversion of vascular smooth muscle cells to bone-like cells, and the regulatory pathways involved in both bone and vessel mineralization. Further elucidation of the mechanisms underlying the calcification paradox is crucial in order to develop preventive and therapeutic strategies to deal with vascular calcification and reduce the associated cardiovascular risk.
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