Pathophysiology of vascular calcification
NX Chen, SM Moe - Current osteoporosis reports, 2015 - Springer
NX Chen, SM Moe
Current osteoporosis reports, 2015•SpringerVascular calcification can lead to cardiovascular morbidity and mortality. The initiating
factors and clinical consequences depend on the underlying disease state and location of
the calcification. The pathogenesis of vascular calcification is complex and involves a
transformation of vascular smooth muscle cells to an osteo/chondrocytic cell that expresses
RUNX2 and produces matrix vesicles. The imbalance of promoters (such as
hyperphosphatemia and hypercalcemia) and inhibitors (eg, fetuin-A) is critical in the …
factors and clinical consequences depend on the underlying disease state and location of
the calcification. The pathogenesis of vascular calcification is complex and involves a
transformation of vascular smooth muscle cells to an osteo/chondrocytic cell that expresses
RUNX2 and produces matrix vesicles. The imbalance of promoters (such as
hyperphosphatemia and hypercalcemia) and inhibitors (eg, fetuin-A) is critical in the …
Abstract
Vascular calcification can lead to cardiovascular morbidity and mortality. The initiating factors and clinical consequences depend on the underlying disease state and location of the calcification. The pathogenesis of vascular calcification is complex and involves a transformation of vascular smooth muscle cells to an osteo/chondrocytic cell that expresses RUNX2 and produces matrix vesicles. The imbalance of promoters (such as hyperphosphatemia and hypercalcemia) and inhibitors (e.g., fetuin-A) is critical in the development of vascular calcification. The altered mineral metabolism and deficiency in inhibitors are common in patients with chronic kidney disease (CKD) and is one reason why vascular calcification is so prevalent in that population.
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