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The TBX1 Transcription Factor in Cardiac Remodeling After Myocardial Infarction

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dc.contributor.authorSanchez Mas, Jesus
dc.contributor.authorLax Pérez, Antonio Manuel
dc.contributor.authorAsensio Lopez, Maria del Carmen
dc.contributor.authorFernandez del Palacio, Maria J
dc.contributor.authorCaballero, Luis
dc.contributor.authorNavarro-Peñalver, Marina
dc.contributor.authorPerez Martinez, Maria T
dc.contributor.authorGimeno Blanes, Juan R
dc.contributor.authorPascual Figal, Domingo A.
dc.contributor.departmentMedicina
dc.date.accessioned2024-01-23T13:08:45Z
dc.date.available2024-01-23T13:08:45Z
dc.date.issued2016-11
dc.description.abstractIntroduction and objectives: The transcription factor TBX1 plays an important role in the embryonic development of the heart. Nothing is known about its involvement in myocardial remodeling after acute myocardial infarction (AMI) and whether its expression can be modulated by a treatment with proven benefit such as mineralocorticoid receptor blockade. Methods: Acute myocardial infarction was induced in 60 rats via left coronary artery ligation: 50 animals were randomized to be euthanized after 1, 2, 4, 12, or 24 weeks; 10 animals were treated with eplerenone (100 mg/kg/days) 7 days before the AMI until their euthanasia (4 weeks later); 8 additional animals underwent surgery without ligation (control). We analyzed the cardiac expression of TBX1, fetal genes, and fibrosis markers. Results: The gene and protein expression of TBX1 was increased in the infarcted myocardium, peaking 1 week after AMI (P < .01), without changes in the noninfarcted myocardium. Levels of the fetal genes and fibrosis markers also increased, peaking 4 weeks (P < .001) and 1 week (P < .01) after AMI, respectively. The TBX1 expression was correlated with that of the fibrosis markers (P < .01) but not the fetal genes. Eplerenone reduced the TBX1 increase and fibrosis induced by AMI, with an association improvement in ventricular function and remodeling in echocardiography. Conclusions: These results show the reactivated expression of TBX1 and indicate its involvement in cardiac fibrosis and remodeling after AMI and its participation in the benefit from mineralocorticoid receptor blockade.es
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dc.format.extent9es
dc.identifier.citationRev Esp Cardiol (Engl Ed). 2016 Nov 69(11):1042-1050.doi: 10.1016/j.rec.2016.04.033. Epub 2016 Jul 12.
dc.identifier.doi10.1016/j.rec.2016.04.033
dc.identifier.urihttp://hdl.handle.net/10201/137619
dc.languageenges
dc.relationThis work has been funded by the Fundación Séneca-Agencia de Ciencia y Tecnología of the Region of Murcia (19334/PI/14), the Instituto de Salud Carlos III, Madrid (PI14/01637), and the Red de Investigación Cardiovascular (RIC), Ministerio de Sanidad y Consumo, Madrid, Spain (RD12/0042/0049).es
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectAcute myocardial infarctiones
dc.subjectCardiac remodelinges
dc.subjectFibrosises
dc.subjectFetal geneses
dc.subjectEplerenonees
dc.titleThe TBX1 Transcription Factor in Cardiac Remodeling After Myocardial Infarctiones
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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