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Endogenous calcification inhibitors in the prevention of vascular calcification: a consensus statement from the COST action EuroSoftCalcNet

dc.contributor.authorBäck, Magnus
dc.contributor.authorAranyi, Tamas
dc.contributor.authorCancela, M. Leonor
dc.contributor.authorCarracedo, Miguel
dc.contributor.authorConceição, Natércia
dc.contributor.authorLeftheriotis, Georges
dc.contributor.authorMacrae, Vicky
dc.contributor.authorMartin, Ludovic
dc.contributor.authorNitschke, Yvonne
dc.contributor.authorPasch, Andreas
dc.contributor.authorQuaglino, Daniela
dc.contributor.authorRutsch, Frank
dc.contributor.authorShanahan, Catherine
dc.contributor.authorSorribas, Victor
dc.contributor.authorSzeri, Flora
dc.contributor.authorValdivielso, Pedro
dc.contributor.authorVanakker, Olivier
dc.contributor.authorKempf, Hervé
dc.date.accessioned2019-05-21T10:40:34Z
dc.date.available2019-05-21T10:40:34Z
dc.date.issued2019-01
dc.description.abstractThe physicochemical deposition of calcium-phosphate in the arterial wall is prevented by calcification inhibitors. Studies in cohorts of patients with rare genetic diseases have shed light on the consequences of loss-of-function mutations for different calcification inhibitors, and genetic targeting of these pathways in mice have generated a clearer picture on the mechanisms involved. For example, generalized arterial calcification of infancy (GACI) is caused by mutations in the enzyme ecto-nucleotide pyrophosphatase/phosphodiesterase-1 (eNPP1), preventing the hydrolysis of ATP into pyrophosphate (PPi). The importance of PPi for inhibiting arterial calcification has been reinforced by the protective effects of PPi in various mouse models displaying ectopic calcifications. Besides PPi, Matrix Gla Protein (MGP) has been shown to be another potent calcification inhibitor as Keutel patients carrying a mutation in the encoding gene or Mgp-deficient mice develop spontaneous calcification of the arterial media. Whereas PPi and MGP represent locally produced calcification inhibitors, also systemic factors contribute to protection against arterial calcification. One such example is Fetuin-A, which is mainly produced in the liver and which forms calciprotein particles (CPPs), inhibiting growth of calcium-phosphate crystals in the blood and thereby preventing their soft tissue deposition. Other calcification inhibitors with potential importance for arterial calcification include osteoprotegerin, osteopontin, and klotho. The aim of the present review is to outline the latest insights into how different calcification inhibitors prevent arterial calcification both under physiological conditions and in the case of disturbed calcium-phosphate balance, and to provide a consensus statement on their potential therapeutic role for arterial calcification.pt_PT
dc.description.sponsorshipAgência financiadora COST action - CA16115 EuroSoftCalcNetpt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.doi10.3389/fcvm.2018.00196pt_PT
dc.identifier.issn2297-055X
dc.identifier.urihttp://hdl.handle.net/10400.1/12534
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherFrontiers Mediapt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectArterial calcificationpt_PT
dc.subjectPyrophosphatept_PT
dc.subjectGla proteinspt_PT
dc.subjectKlothopt_PT
dc.subjectOsteoprotegerinpt_PT
dc.subjectOsteopontinpt_PT
dc.subjectFetuinpt_PT
dc.titleEndogenous calcification inhibitors in the prevention of vascular calcification: a consensus statement from the COST action EuroSoftCalcNetpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.startPage196pt_PT
oaire.citation.titleFrontiers in Cardiovascular Medicinept_PT
oaire.citation.volume5pt_PT
person.familyNameCancela
person.familyNameConceição
person.givenNameM. Leonor
person.givenNameNatércia
person.identifier.ciencia-id7C11-760D-F425
person.identifier.orcid0000-0003-3114-6662
person.identifier.orcid0000-0002-5057-0912
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublicationb9bbfe32-3dfe-4131-ad14-a4394008447f
relation.isAuthorOfPublication62064ac0-1f34-407d-96b7-b7074325a84e
relation.isAuthorOfPublication.latestForDiscovery62064ac0-1f34-407d-96b7-b7074325a84e

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