dc.contributor.author | Bentzon, Jacob F | |
dc.contributor.author | Majesky, Mark W | |
dc.date.accessioned | 2020-05-07T10:39:15Z | |
dc.date.available | 2020-05-07T10:39:15Z | |
dc.date.issued | 2018-03 | |
dc.identifier.citation | Cardiovasc Res. 2018; 114(4):492-500 | es_ES |
dc.identifier.issn | 0008-6363 | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/9945 | |
dc.description.abstract | Advances in lineage-tracking techniques have provided new insights into the origins and fates of smooth muscle cells (SMCs) in atherosclerosis. Yet new tools present new challenges for data interpretation that require careful consideration of the strengths and weaknesses of the methods employed. At the same time, discoveries in other fields have introduced new perspectives on longstanding questions about steps in atherogenesis that remain poorly understood. In this article, we address both the challenges and opportunities for a better understanding of the mechanisms by which cells appearing as or deriving from SMCs accumulate in atherosclerosis. | es_ES |
dc.description.sponsorship | J.F.B. was supported by research grants from the Danish Council for Independent Research (Sapere Aude II, 4004-00459B) and the Ministerio de Economia, Industria y Competitividad (MEIC; Programa RETOS, SAF2016-75580-R) with cofunding by Fondo Europeo de Desarrollo Regional (FEDER). The CNIC was supported by MEIC and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (MINECO award SEV-2015-0505). M.W.M. was supported by research grants from the National Institutes of Health (RO1-HL123650, and RO1-HL121877), the Loie Power Robinson Stem Cell & Regenerative Medicine Fund, and the Seattle Children's Research Institute, Seattle, WA. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Oxford University Press | es_ES |
dc.type.hasVersion | AM | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject.mesh | Actins | es_ES |
dc.subject.mesh | Animals | es_ES |
dc.subject.mesh | Atherosclerosis | es_ES |
dc.subject.mesh | Biomarkers | es_ES |
dc.subject.mesh | Gene Expression Regulation, Developmental | es_ES |
dc.subject.mesh | Humans | es_ES |
dc.subject.mesh | Muscle, Smooth, Vascular | es_ES |
dc.subject.mesh | Myocytes, Smooth Muscle | es_ES |
dc.subject.mesh | Neovascularization, Physiologic | es_ES |
dc.subject.mesh | Phenotype | es_ES |
dc.subject.mesh | Signal Transduction | es_ES |
dc.subject.mesh | Cell Differentiation | es_ES |
dc.subject.mesh | Cell Lineage | es_ES |
dc.title | Lineage tracking of origin and fate of smooth muscle cells in atherosclerosis | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.identifier.pubmedID | 29293902 | es_ES |
dc.format.volume | 114 | es_ES |
dc.format.number | 4 | es_ES |
dc.format.page | 492-500 | es_ES |
dc.identifier.doi | 10.1093/cvr/cvx251 | es_ES |
dc.contributor.funder | Danish Council for Independent Research | |
dc.contributor.funder | Ministerio de Economía, Industria y Competitividad (España) | |
dc.contributor.funder | Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) | |
dc.contributor.funder | Fundación ProCNIC | |
dc.contributor.funder | National Institutes of Health (Estados Unidos) | |
dc.description.peerreviewed | Sí | es_ES |
dc.identifier.e-issn | 1755-3245 | es_ES |
dc.relation.publisherversion | https://doi.org/10.1093/cvr/cvx251 | es_ES |
dc.identifier.journal | Cardiovascular research | es_ES |
dc.repisalud.orgCNIC | CNIC::Grupos de investigación::Patología Experimental de la Aterosclerosis | es_ES |
dc.repisalud.institucion | CNIC | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/SEV-2015-0505 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/SAF2016-75580-R | es_ES |
dc.rights.accessRights | open access | es_ES |