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dc.contributor.authorIzidoro, Mario Augusto
dc.contributor.authorCecconi, Alberto
dc.contributor.authorPanadero, María Isabel
dc.contributor.authorMateo, Jesus 
dc.contributor.authorGodzien, Joanna
dc.contributor.authorVilchez, Jean Paul 
dc.contributor.authorLópez-Gonzálvez, Ángeles
dc.contributor.authorRuiz-Cabello, Jesus 
dc.contributor.authorIbanez, Borja 
dc.contributor.authorBarbas, Coral
dc.contributor.authorRupérez, Francisco J
dc.identifier.citationSci Rep. 2020; 10(1):7072es_ES
dc.description.abstractBalloon catheter endothelial denudation in New Zealand white rabbits fed high cholesterol diet is a validated atherosclerosis model. Well-characterized in terms of atherosclerosis induction and progression, the metabolic changes associated with the atherosclerosis progression remain indeterminate. Non-targeted metabolomics permits to develop such elucidation and allows to evaluate the metabolic consequences of colchicine treatment, an anti-inflammatory drug that could revert these changes. 16 rabbits underwent 18 weeks of atherosclerosis induction by diet and aortic denudation. Thereafter animals were randomly assigned to colchicine treatment or placebo for 18 weeks while on diet. Plasma samples were obtained before randomization and at 36 weeks. Multiplatform (GC/MS, CE/MS, RP-HPLC/MS) metabolomics was applied. Plasma fingerprints were pre-processed, and the resulting matrixes analyzed to unveil differentially expressed features. Different chemical annotation strategies were accomplished for those significant features. We found metabolites associated with either atherosclerosis progression, or colchicine treatment, or both. Atherosclerosis was profoundly associated with an increase in circulating bile acids. Most of the changes associated with sterol metabolism could not be reverted by colchicine treatment. However, the variations in lysine, tryptophan and cysteine metabolism among others, have shown new potential mechanisms of action of the drug, also related to atherosclerosis progression, but not previously described.es_ES
dc.description.sponsorshipM.A.I. received funding from Airbus Defense and Space through the CLX-2 program developed with Comando da Aeronáutica (COMAER) and the Brazilian Government. This work has been partially funded by the Ministerio de Ciencia, Innovación y Universidades of Spain (MICINN RTI2018-095166-B-I00), the Spanish Society of Cardiology (“Proyecto investigación traslacional” to BI), the Carlos III Institute of Health (ISCiii FIS-FEDER PI14-01427 to JM), the Ministerio de Economía, Industria y Competitividad (MINECO SAF2017-84494-C2-1R to JR-C), a project granted by the BBVA Foundation to JR-C. This work was performed under the Maria de Maeztu Units of Excellence Program from the Spanish State Research Agency (MDM-2017-0720). The CNIC is supported by the ISCiii, and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (SEV-2015-0505).es_ES
dc.publisherNature Researches_ES
dc.relation.isversionofPublisher's versiones_ES
dc.titlePlasma Metabolic Signature of Atherosclerosis Progression and Colchicine Treatment in Rabbits.es_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.contributor.funderAirbus Defense and Spacees_ES
dc.contributor.funderMinisterio de Ciencia, Innovación y Universidades (España)es_ES
dc.contributor.funderSociedad Española de Cardiologíaes_ES
dc.contributor.funderMinisterio de Economía, Industria y Competitividad (España)es_ES
dc.contributor.funderFundación BBVAes_ES
dc.contributor.funderFundación ProCNICes_ES
dc.identifier.journalScientific reportses_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Laboratorio Traslacional para la Imagen y Terapia Cardiovasculares_ES
dc.repisalud.orgCNICCNIC::Unidades técnicas::Imagen Avanzadaes_ES

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