<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>0120-5633</journal-id>
<journal-title><![CDATA[Revista Colombiana de Cardiología]]></journal-title>
<abbrev-journal-title><![CDATA[Rev. Colomb. Cardiol.]]></abbrev-journal-title>
<issn>0120-5633</issn>
<publisher>
<publisher-name><![CDATA[Sociedad Colombiana de Cardiologia. Oficina de Publicaciones]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0120-56332017000200146</article-id>
<article-id pub-id-type="doi">10.1016/j.rccar.2016.04.019</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Perspectivas moleculares en cardiopatía hipertrófica: abordaje epigenético desde la modificación de la cromatina]]></article-title>
<article-title xml:lang="en"><![CDATA[Molecular perspectives in hypertrophic cardiomyopathy: epigenetic approach from chromatin remodeling]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Hernández]]></surname>
<given-names><![CDATA[Angélica]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Duque]]></surname>
<given-names><![CDATA[Juan]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Rosales]]></surname>
<given-names><![CDATA[Wendy]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Lizcano]]></surname>
<given-names><![CDATA[Fernando]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad de La Sabana Centro de Investigación Biomédica ]]></institution>
<addr-line><![CDATA[Chía ]]></addr-line>
<country>Colombia</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Fundación Cardioinfantil-Instituto de Cardiología  ]]></institution>
<addr-line><![CDATA[Bogotá ]]></addr-line>
<country>Colombia</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>04</month>
<year>2017</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>04</month>
<year>2017</year>
</pub-date>
<volume>24</volume>
<numero>2</numero>
<fpage>146</fpage>
<lpage>152</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_arttext&amp;pid=S0120-56332017000200146&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_abstract&amp;pid=S0120-56332017000200146&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_pdf&amp;pid=S0120-56332017000200146&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen Los cambios epigenéticos inducidos por factores ambientales tienen cada día más relevancia en las enfermedades cardiovasculares. Uno de los componentes moleculares más observados en la hipertrofia cardiaca es la reactivación de los genes fetales causados por diversas patologías que incluyen obesidad, hipertensión arterial, estenosis valvular aórtica, causas congénitas, entre otras. A pesar de las múltiples investigaciones cuyo objetivo es obtener información acerca de los componentes moleculares de esta patología, su influencia en las estrategias terapéuticas es relativamente escasa. En la actualidad se busca información acerca de las proteínas que modifican la expresión de los genes fetales que se reactivan en esta condición. La relación entre las histonas y el ADN tiene un control reconocido en la expresión de genes que son condicionados por el ambiente e inducen modificaciones epigenéticas. Las deacetilasas de histonas son un grupo de proteínas que han demostrado tener un papel importante en la diferenciación de la célula cardiaca y además pueden ser claros componentes en el desarrollo de la hipertrofia cardiaca. En este trabajo se revisan los conocimientos actuales sobre la influencia de estas proteínas y los posibles planes terapéuticos en la hipertrofia cardiaca.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Epigenetic alterations induced by environmental factors are more relevant each day for cardiovascular diseases. One of the most observed molecular components in hypertrophic cardiomyopathy is the reactivation of fetal genes caused by multiple conditions, including obesity, high blood pressure, aortic valve stenosis and congenital causes. Despite several investigations with the objective of obtaining information regarding molecular components of this condition, its influence in therapeutic strategies is relatively scarce. Nowadays information is being searched about proteins that modify the expression of the fetal genes that reactivate with this condition. The relationship between histones and DNA has a recognised control in the expression of genes that are subject to the environment and induce epigenetic alterations. Histone deacetylases are a group of proteins that have revealed to play an important role in differentiation the cardiac cell and could be clear components in the development of hypertrophic cardiomyopathy. In this study current knowledge about the influence of these proteins and possible therapeutic plans for hypertrophic cardiomyopathy are revised.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Hipertrofia cardiaca]]></kwd>
<kwd lng="es"><![CDATA[Epigenétxica]]></kwd>
<kwd lng="es"><![CDATA[Demetilación de histonas]]></kwd>
<kwd lng="en"><![CDATA[Hypertrophic cardiomyopathy]]></kwd>
<kwd lng="en"><![CDATA[Epigenetics]]></kwd>
<kwd lng="en"><![CDATA[Histone methylation]]></kwd>
</kwd-group>
</article-meta>
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