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Molecular perspectives in hypertrophic heart disease: An epigenetic approach from chromatin modification
dc.contributor.advisor | Lizcano, Fernando | |
dc.creator | Bustamante Gómez, Lizeth Viviana | |
dc.creator.degree | Especialista en Endocrinología | |
dc.creator.degreeLevel | Maestría | |
dc.creator.degreetype | Full time | |
dc.date.accessioned | 2024-08-22T19:31:32Z | |
dc.date.available | 2024-08-22T19:31:32Z | |
dc.date.created | 2023-01-18 | |
dc.description | Los cambios epigenéticos inducidos por factores ambientales son cada vez más relevantes en las enfermedades cardiovasculares. El componente molecular más frecuente en la hipertrofia cardíaca es la reactivación de genes fetales causada por diversas patologías, entre ellas obesidad, hipertensión arterial, estenosis de la válvula aórtica y causas congénitas. A pesar de las múltiples investigaciones realizadas para lograr información sobre los componentes moleculares de esta patología, su influencia en las estrategias terapéuticas es relativamente escasa. Recientemente se ha obtenido nueva información sobre las proteínas que modifican la expresión de genes fetales reactivados en la hipertrofia cardíaca. Estas proteínas modifican el ADN de forma covalente e inducen cambios en la estructura de la cromatina. La relación entre histonas y ADN tiene un reconocido control en la expresión de genes condicionado por el ambiente e induce variaciones epigenéticas. Las modificaciones epigenéticas que regulan la hipertrofia cardíaca patológica se realizan mediante cambios en la estabilidad genómica, la arquitectura de la cromatina y la expresión genética. La trimetilación de la histona 3 en la lisina 4, 9 o 27 (H3-K4; -K9; -K27me3) y la desmetilación de la histona en la lisina 9 y 79 (H3-K9; -K79) son mediadores de la reprogramación en la hipertrofia patológica. Dentro de los modificadores de la arquitectura de la cromatina, las histonas desmetilasas son un grupo de proteínas que se ha demostrado que desempeñan un papel esencial en la diferenciación de las células cardíacas y también pueden ser componentes en el desarrollo de la hipertrofia cardíaca. En el presente trabajo se revisa el conocimiento actual sobre la influencia de las modificaciones epigenéticas en la expresión de genes implicados en la hipertrofia cardíaca y su posible abordaje terapéutico. | |
dc.description.abstract | Epigenetic changes induced by environmental factors are increasingly relevant in cardiovascular diseases. The most frequent molecular component in cardiac hypertrophy is the reactivation of fetal genes caused by various pathologies, including obesity, arterial hypertension, aortic valve stenosis, and congenital causes. Despite the multiple investigations performed to achieve information about the molecular components of this pathology, its influence on therapeutic strategies is relatively scarce. Recently, new information has been taken about the proteins that modify the expression of fetal genes reactivated in cardiac hypertrophy. These proteins modify the DNA covalently and induce changes in the structure of chromatin. The relationship between histones and DNA has a recognized control in the expression of genes conditioned by the environment and induces epigenetic variations. The epigenetic modifications that regulate pathological cardiac hypertrophy are performed through changes in genomic stability, chromatin architecture, and gene expression. Histone 3 trimethylation at lysine 4, 9, or 27 (H3-K4; -K9; -K27me3) and histone demethylation at lysine 9 and 79 (H3-K9; -K79) are mediators of reprogramming in pathologic hypertrophy. Within the chromatin architecture modifiers, histone demethylases are a group of proteins that have been shown to play an essential role in cardiac cell differentiation and may also be components in the development of cardiac hypertrophy. In the present work, we review the current knowledge about the influence of epigenetic modifications in the expression of genes involved in cardiac hypertrophy and its possible therapeutic approach. | |
dc.format.extent | 11 pp | |
dc.format.mimetype | application/pdf | |
dc.identifier.doi | https://doi.org/10.3389/fcell.2022.1070338 | |
dc.identifier.uri | https://repository.urosario.edu.co/handle/10336/43309 | |
dc.language.iso | eng | |
dc.publisher | Universidad del Rosario | |
dc.publisher.department | Escuela de Medicina y Ciencias de la Salud | |
dc.publisher.program | Especialización en Endocrinología | |
dc.relation.uri | https://www.frontiersin.org/journals/cell-and-developmental-biology/articles/10.3389/fcell.2022.1070338/full | |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 International | * |
dc.rights.accesRights | info:eu-repo/semantics/closedAccess | |
dc.rights.acceso | Bloqueado (Texto referencial) | |
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dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
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dc.source.instname | instname:Universidad del Rosario | |
dc.source.reponame | reponame:Repositorio Institucional EdocUR | |
dc.subject | Epigenetica | |
dc.subject | Enfermedad cardiaca hipertrofica | |
dc.subject | Modificaciones de la cromatina | |
dc.subject.keyword | Epigenetic | |
dc.subject.keyword | Hypertrophic heart disease | |
dc.subject.keyword | Chromatin modification | |
dc.title | Molecular perspectives in hypertrophic heart disease: An epigenetic approach from chromatin modification | |
dc.title.TranslatedTitle | Perspectivas Moleculares en la enfermedad Cardiaca hipertrofica: un abordajes epigenetico desde las modificaciones de la cromatina | |
dc.type | bachelorThesis | |
dc.type.document | Artículo | |
dc.type.hasVersion | info:eu-repo/semantics/acceptedVersion | |
dc.type.spa | Artículo | |
local.department.report | Escuela de Medicina y Ciencias de la Salud | |
local.regiones | Bogotá |
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