The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.
Vascular Calcification: In Vitro Evidence for the Role of Inorganic Phosphate
Abstract
Uremic patients are prone to widespread ectopic extraskeletal calcification resulting from an imbalance of systemic inorganic phosphate (Pi). There can be serious consequences of this process, particularly when it results in the calcification of the vasculature. A recent study examined the response of cultured human aortic smooth muscle cells to varying levels of extracellular Pi. Cells that were exposed to Pi levels similar to those seen in uremic patients (>1.4 mmol/L) showed dose-dependent increases in cell culture calcium deposition. The results of this study also defined the role of elevated phosphate in transforming the vascular phenotype of these cells to an osteogenic phenotype, such that a predisposition for calcification was created. Pi-induced changes included increased expression of the osteogenic markers osteocalcin and core-binding factor-1 genes, the latter of which is considered a "master gene" critical for osteoblast differentiation. These changes occur early after exposure to high phosphate levels and seem to be mediated by a sodium-dependent phosphate co-transporter, Pit-1 (Glvr-1). Calcification of vascular cells also seems to occur in the absence of a mineral imbalance but in the presence of platelet-derived growth factor, a potent atherogenic factor. Taken together, these data suggest that calcification of vascular cells can occur early in a phosphate-rich environment similar to that seen in patients with renal failure and in a platelet-derived growth factor-rich atherosclerotic region under normal phosphorus conditions. From a clinical viewpoint, it seems that early control or prevention of hyperphosphatemia may reduce coronary calcification and its associated morbidity and mortality for patients on dialysis.
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Phosphate Regulation of Vascular Smooth Muscle Cell Calcification
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Self-citationArterial Calcifications, Arterial Stiffness, and Cardiovascular Risk in End-Stage Renal Disease
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Cited by
Murshed, M., Harmey, D., Millán, J. L., McKee, M. D., & Karsenty, G. (2005) · Genes & Development · doi:10.1101/gad.1276205 · Cited by 601
Pathophysiology of Vascular Calcification in Chronic Kidney Disease
Moe, S. M., & Chen, N. X. (2004) · Circulation Research · doi:10.1161/01.res.0000141775.67189.98 · Cited by 502
The emerging role of phosphate in vascular calcification
Giachelli, C. M. (2009) · Kidney International · doi:10.1038/ki.2008.644 · Cited by 493
Self-citationRegulation of Vascular Calcification by Osteoclast Regulatory Factors RANKL and Osteoprotegerin
Collin-Osdoby, P. (2004) · Circulation Research · doi:10.1161/01.res.0000149165.99974.12 · Cited by 473
Mechanistic Insights into Vascular Calcification in CKD
Shroff, R., Long, D. A., & Shanahan, C. (2013) · Journal of the American Society of Nephrology · doi:10.1681/asn.2011121191 · Cited by 396
Metadata
- Authors
- Giachelli, C. M.
- Venue
- Journal of the American Society of Nephrology
- Published
- 2003-09
- Volume
- 14
- Issue
- suppl_4
- Pages
- S300-S304
- ISSN
- 1046-6673 (ISSN-L)
- OpenAlex
- W2160745333
- Cited by
- 284
- References
- 32
- FWCI
- 8.66
- Type
- journal article
- Language
- en
- Open access
- closed
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