Regulation of the sodium-phosphate cotransporter Pit-1 and its role in vascular calcification
Author
dc.contributor.author
González, Magdalena
Author
dc.contributor.author
Martínez, Rafael
Author
dc.contributor.author
Amador, Cristián
Author
dc.contributor.author
Michea Acevedo, Luis
Admission date
dc.date.accessioned
2019-03-11T12:58:15Z
Available date
dc.date.available
2019-03-11T12:58:15Z
Publication date
dc.date.issued
2009
Cita de ítem
dc.identifier.citation
Current Vascular Pharmacology, Volumen 7, Issue 4, 2018, Pages 506-512
Identifier
dc.identifier.issn
15701611
Identifier
dc.identifier.other
10.2174/157016109789043946
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/164849
Abstract
dc.description.abstract
Vascular calcification is caused by the deposition of basic calcium phosphate crystals in blood vessels, myocardium, and/or cardiac valves. Calcification decreases artery wall compliance, and arterial calcification is associated to mortality in hyperphosphatemic renal failure and diabetes mellitus. The calcification of the tunica media characterizes the arteriosclerosis observed with age, diabetes and end stage-renal disease, and it can develop independently from intima calcification. As part of the vascular calcification mechanism, vascular smooth muscle cells (VSMC) experience a transition from a contractile to an osteochondrogenic phenotype and a sequence of molecular events that are typical of endochondral ossification. The current evidence indicates a key role of increased phosphate uptake by VSMC for calcification, which supplies the substrate for hydroxyapatite formation and could trigger or potentiate VSMC transdiferentiation. The present review analyzes the sodium-phosphate co