Mostrar el registro sencillo del ítem
dc.contributor.author | González-Santamaría, José | |
dc.contributor.author | Villalba, María | |
dc.contributor.author | Busnadiego, Oscar | |
dc.contributor.author | Lopez-Olaneta, Marina | |
dc.contributor.author | Sandoval, Pilar | |
dc.contributor.author | Snabel, Jessica | |
dc.contributor.author | López-Cabrera, Manuel | |
dc.contributor.author | Erler, Janine T | |
dc.contributor.author | Hanemaaijer, Roeland | |
dc.contributor.author | Lara-Pezzi, Enrique | |
dc.contributor.author | Rodríguez-Pascual, Fernando | |
dc.date.accessioned | 2019-07-29T14:48:47Z | |
dc.date.available | 2019-07-29T14:48:47Z | |
dc.date.issued | 2016-01 | |
dc.identifier.citation | Cardiovasc Res. 2016; 109(1):67-78 | es_ES |
dc.identifier.issn | 0008-6363 | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/7985 | |
dc.description.abstract | AIMS: After myocardial infarction (MI), extensive remodelling of the extracellular matrix contributes to scar formation. While aiming to preserve tissue integrity, this fibrotic response is also associated with adverse events, including a markedly increased risk of heart failure, ventricular arrhythmias, and sudden cardiac death. Cardiac fibrosis is characterized by extensive deposition of collagen and also by increased stiffness as a consequence of enhanced collagen cross-linking. Members of the lysyl oxidase (LOX) family of enzymes are responsible for the formation of collagen cross-links. This study investigates the contribution of LOX family members to the heart response to MI. METHODS AND RESULTS: Experimental MI was induced in C57BL/6 mice by permanent ligation of the left anterior descending coronary artery. The expression of LOX isoforms (LOX and LOXL1-4) was strongly increased upon MI, and this response was accompanied by a significant accumulation of mature collagen fibres in the infarcted area. LOX expression was observed in areas of extensive remodelling, partially overlapping with α-smooth muscle actin-expressing myofibroblasts. Tumour growth factor-β as well as hypoxia-activated pathways contributed to the induction of LOX expression in cardiac fibroblasts. Finally, in vivo post-infarction treatment with the broadband LOX inhibitor β-aminopropionitrile or, selectively, with a neutralizing antibody against the canonical LOX isoform attenuated collagen accumulation and maturation and also resulted in reduced ventricular dilatation and improved cardiac function. CONCLUSION: LOX family members contribute significantly to the detrimental effects of cardiac remodelling, highlighting LOX inhibition as a potential therapeutic strategy for post-infarction recovery. | es_ES |
dc.description.sponsorship | Ministerio de Economia y Competitividad (Plan Nacional de I+D+I) [SAF2012-34916, SAF2012-31451]; Comunidad Autonoma de Madrid (FIBROTEAM Consortium) [2010-BMD2321]; European Union's FP7 [ERG-239158, CardioNeT-ITN-289600, CardioNext-ITN-608027]; Ministerio de Economia y Competitividad (Formacion de Personal Investigador) | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | European Society of Cardiology (ESC) | es_ES |
dc.type.hasVersion | AM | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-sa/4.0/ | * |
dc.subject | Cardiac fibrosis | es_ES |
dc.subject | Collagen | es_ES |
dc.subject | Lysyl oxidases | es_ES |
dc.subject | Myocardial infarction | es_ES |
dc.subject | Myofibroblast | es_ES |
dc.subject.mesh | Animals | es_ES |
dc.subject.mesh | Cell Hypoxia | es_ES |
dc.subject.mesh | Cells, Cultured | es_ES |
dc.subject.mesh | Enzyme Induction | es_ES |
dc.subject.mesh | Extracellular Matrix | es_ES |
dc.subject.mesh | Heart | es_ES |
dc.subject.mesh | Mice | es_ES |
dc.subject.mesh | Mice, Inbred C57BL | es_ES |
dc.subject.mesh | Myocardial Infarction | es_ES |
dc.subject.mesh | Protein-Lysine 6-Oxidase | es_ES |
dc.subject.mesh | Transforming Growth Factor beta | es_ES |
dc.title | Matrix cross-linking lysyl oxidases are induced in response to myocardial infarction and promote cardiac dysfunction | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Atribución-NoComercial-CompartirIgual 4.0 Internacional | * |
dc.identifier.pubmedID | 26260798 | es_ES |
dc.format.volume | 109 | es_ES |
dc.format.number | 1 | es_ES |
dc.format.page | 67-78 | es_ES |
dc.identifier.doi | 10.1093/cvr/cvv214 | es_ES |
dc.contributor.funder | Ministerio de Economía y Competitividad (España) | |
dc.contributor.funder | Comunidad de Madrid (España) | |
dc.contributor.funder | Unión Europea. Comisión Europea | |
dc.description.peerreviewed | Sí | es_ES |
dc.identifier.e-issn | 1755-3245 | es_ES |
dc.relation.publisherversion | https://doi.org/10.1093/cvr/cvv214 | es_ES |
dc.identifier.journal | Cardiovascular research | es_ES |
dc.repisalud.orgCNIC | CNIC::Grupos de investigación::Regulación Molecular de la Insuficiencia Cardiaca | es_ES |
dc.repisalud.institucion | CNIC | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/EC/FP7/289600/EU | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/EC/FP7/608027/EU | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/SAF2012-34916 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/SAF2012-31451 | es_ES |
dc.rights.accessRights | open access | es_ES |