Molecular perspectives in hypertrophic heart disease: An epigenetic approach from chromatin modification

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 arter...

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Fecha de publicación:: 2023

Institución:: Universidad del Rosario

Repositorio:: Repositorio EdocUR - U. Rosario

Idioma:: eng

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dc.title.none.fl_str_mv	Molecular perspectives in hypertrophic heart disease: An epigenetic approach from chromatin modification
dc.title.TranslatedTitle.none.fl_str_mv	Perspectivas Moleculares en la enfermedad Cardiaca hipertrofica: un abordajes epigenetico desde las modificaciones de la cromatina
title	Molecular perspectives in hypertrophic heart disease: An epigenetic approach from chromatin modification
spellingShingle	Molecular perspectives in hypertrophic heart disease: An epigenetic approach from chromatin modification Epigenetica Enfermedad cardiaca hipertrofica Modificaciones de la cromatina Epigenetic Hypertrophic heart disease Chromatin modification
title_short	Molecular perspectives in hypertrophic heart disease: An epigenetic approach from chromatin modification
title_full	Molecular perspectives in hypertrophic heart disease: An epigenetic approach from chromatin modification
title_fullStr	Molecular perspectives in hypertrophic heart disease: An epigenetic approach from chromatin modification
title_full_unstemmed	Molecular perspectives in hypertrophic heart disease: An epigenetic approach from chromatin modification
title_sort	Molecular perspectives in hypertrophic heart disease: An epigenetic approach from chromatin modification
dc.contributor.advisor.none.fl_str_mv	Lizcano, Fernando
dc.subject.none.fl_str_mv	Epigenetica Enfermedad cardiaca hipertrofica Modificaciones de la cromatina
topic	Epigenetica Enfermedad cardiaca hipertrofica Modificaciones de la cromatina Epigenetic Hypertrophic heart disease Chromatin modification
dc.subject.keyword.none.fl_str_mv	Epigenetic Hypertrophic heart disease Chromatin modification
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.
publishDate	2023
dc.date.created.none.fl_str_mv	2023-01-18
dc.date.accessioned.none.fl_str_mv	2024-08-22T19:31:32Z
dc.date.available.none.fl_str_mv	2024-08-22T19:31:32Z
dc.type.none.fl_str_mv	bachelorThesis
dc.type.coar.fl_str_mv	http://purl.org/coar/resource_type/c_7a1f
dc.type.document.none.fl_str_mv	Artículo
dc.type.spa.none.fl_str_mv	Artículo
dc.identifier.doi.none.fl_str_mv	https://doi.org/10.3389/fcell.2022.1070338
dc.identifier.uri.none.fl_str_mv	https://repository.urosario.edu.co/handle/10336/43309
url	https://doi.org/10.3389/fcell.2022.1070338 https://repository.urosario.edu.co/handle/10336/43309
dc.language.iso.none.fl_str_mv	eng
language	eng
dc.relation.uri.none.fl_str_mv	https://www.frontiersin.org/journals/cell-and-developmental-biology/articles/10.3389/fcell.2022.1070338/full
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dc.format.extent.none.fl_str_mv	11 pp
dc.format.mimetype.none.fl_str_mv	application/pdf
dc.publisher.none.fl_str_mv	Universidad del Rosario
dc.publisher.department.none.fl_str_mv	Escuela de Medicina y Ciencias de la Salud
dc.publisher.program.none.fl_str_mv	Especialización en Endocrinología
publisher.none.fl_str_mv	Universidad del Rosario
institution	Universidad del Rosario
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Epigenetic control and cancer: the potential of histone demethylases as therapeutic targets. Pharm. (Basel) 5 (9), 963–990. doi:10.3390/ph5090963 Madsen, A., Hoppner, G., Krause, J., Hirt, M. N., Laufer, S. D., Schweizer, M., et al. (2020). An important role for DNMT3A-mediated DNA methylation in cardiomyocyte metabolism and contractility. Circulation 142 (16), 1562–1578. doi:10.1161/CIRCULATIONAHA.119.044444 Meder, B., Haas, J., Sedaghat-Hamedani, F., Kayvanpour, E., Frese, K., Lai, A., et al. (2017). Epigenome-Wide association study identifies cardiac gene patterning and a novel class of biomarkers for heart failure. Circulation 136 (16), 1528–1544. doi:10.1161/CIRCULATIONAHA.117.027355 Millan-Zambrano, G., Burton, A., Bannister, A. J., and Schneider, R. (2022). Histone post-translational modifications - cause and consequence of genome function. Nat. Rev. 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spelling	Lizcano, Fernando86bcaed1-a8bc-45b8-bcb2-25d353f3d1ac-1Bustamante Gómez, Lizeth VivianaEspecialista en EndocrinologíaMaestríaFull timebcb31556-82de-46be-9ff9-0aa169b50645-12024-08-22T19:31:32Z2024-08-22T19:31:32Z2023-01-18Los 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.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.11 ppapplication/pdfhttps://doi.org/10.3389/fcell.2022.1070338https://repository.urosario.edu.co/handle/10336/43309engUniversidad del RosarioEscuela de Medicina y Ciencias de la SaludEspecialización en Endocrinologíahttps://www.frontiersin.org/journals/cell-and-developmental-biology/articles/10.3389/fcell.2022.1070338/fullAttribution-NonCommercial-NoDerivatives 4.0 InternationalBloqueado (Texto referencial)EL AUTOR, manifiesta que la obra objeto de la presente autorización es original y la realizó sin violar o usurpar derechos de autor de terceros, por lo tanto la obra es de exclusiva autoría y tiene la titularidad sobre la misma. PARGRAFO: En caso de presentarse cualquier reclamación o acción por parte de un tercero en cuanto a los derechos de autor sobre la obra en cuestión, EL AUTOR, asumirá toda la responsabilidad, y saldrá en defensa de los derechos aquí autorizados; para todos los efectos la universidad actúa como un tercero de buena fe. EL AUTOR, autoriza a LA UNIVERSIDAD DEL ROSARIO, para que en los términos establecidos en la Ley 23 de 1982, Ley 44 de 1993, Decisión andina 351 de 1993, Decreto 460 de 1995 y demás normas generales sobre la materia, utilice y use la obra objeto de la presente autorización. -------------------------------------- POLITICA DE TRATAMIENTO DE DATOS PERSONALES. Declaro que autorizo previa y de forma informada el tratamiento de mis datos personales por parte de LA UNIVERSIDAD DEL ROSARIO para fines académicos y en aplicación de convenios con terceros o servicios conexos con actividades propias de la academia, con estricto cumplimiento de los principios de ley. 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Biol. 7 (9), a025064. doi:10.1101/cshperspect.a025064instname:Universidad del Rosarioreponame:Repositorio Institucional EdocUREpigeneticaEnfermedad cardiaca hipertroficaModificaciones de la cromatinaEpigeneticHypertrophic heart diseaseChromatin modificationMolecular perspectives in hypertrophic heart disease: An epigenetic approach from chromatin modificationPerspectivas Moleculares en la enfermedad Cardiaca hipertrofica: un abordajes epigenetico desde las modificaciones de la cromatinabachelorThesisArtículoArtículohttp://purl.org/coar/resource_type/c_7a1fEscuela de Medicina y Ciencias de la SaludBogotáORIGINALMolecular_perspectives_in_hypertrophic_heart_disease.pdfMolecular_perspectives_in_hypertrophic_heart_disease.pdfapplication/pdf5273090https://repository.urosario.edu.co/bitstreams/6536443f-3d8c-4678-ba83-7ab91458e806/downloada8d83012962876bd52a17a512306773cMD51LICENSElicense.txtlicense.txttext/plain1483https://repository.urosario.edu.co/bitstreams/9a723743-349f-4d83-b3da-631c9fa4f797/downloadb2825df9f458e9d5d96ee8b7cd74fde6MD52CC-LICENSElicense_rdflicense_rdfapplication/rdf+xml; charset=utf-8899https://repository.urosario.edu.co/bitstreams/82cc8b73-9b0d-4c95-8fb7-f7c453284b83/download3b6ce8e9e36c89875e8cf39962fe8920MD53TEXTMolecular_perspectives_in_hypertrophic_heart_disease.pdf.txtMolecular_perspectives_in_hypertrophic_heart_disease.pdf.txtExtracted texttext/plain22https://repository.urosario.edu.co/bitstreams/53fd5b04-5816-49a1-a0c8-f8d5c3d3b25f/download6cccda74febad7705949cb89ee2669ddMD54THUMBNAILMolecular_perspectives_in_hypertrophic_heart_disease.pdf.jpgMolecular_perspectives_in_hypertrophic_heart_disease.pdf.jpgGenerated Thumbnailimage/jpeg3446https://repository.urosario.edu.co/bitstreams/7c95304e-093c-4bfb-af8c-6123a6fa160a/download5e7fcec9603e8f0ba812244b0ed30ae7MD5510336/43309oai:repository.urosario.edu.co:10336/433092024-08-23 03:01:37.163http://creativecommons.org/licenses/by-nc-nd/4.0/Attribution-NonCommercial-NoDerivatives 4.0 Internationalhttps://repository.urosario.edu.coRepositorio institucional EdocURedocur@urosario.edu.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

Molecular perspectives in hypertrophic heart disease: An epigenetic approach from chromatin modification

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