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Vascular calcification is a pathological process involving the deposition of calcium salts, mainly hydroxyapatite, in arterial walls. This process is highly regulated biologically and is not simply a passive result of aging or disease[6][5][4]; instead, it involves molecular pathways similar to those in bone formation, with vascular smooth muscle cells adopting osteoblast-like phenotypes and contributing to matrix mineralization[2][6][7]. Vascular calcification is strongly associated with increased cardiovascular risk and is frequently observed in patients with diabetes, atherosclerosis, and chronic kidney disease, as well as those of advanced age[1][3][5]. There is currently no therapy that reverses calcification; treatment focuses on addressing underlying metabolic disorders and risk factors, and on slowing progression using a combination of lifestyle modifications and medication[1][3][8].
Actions are aimed at modulating contributing factors or preventing progression: - Reduction of serum calcium/phosphate - Modulation of inflammatory mediators - Inhibition of vascular smooth muscle cell transdifferentiation to osteoblast-like cells - Inhibition of bone-related signaling pathways (e.g., BMPs, TGF-β, PDGF, Runx2) - Managing underlying risk factors (diabetes, hypertension, CKD)
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