<?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>2529-850X</journal-id>
<journal-title><![CDATA[Journal of Negative and No Positive Results]]></journal-title>
<abbrev-journal-title><![CDATA[JONNPR]]></abbrev-journal-title>
<issn>2529-850X</issn>
<publisher>
<publisher-name><![CDATA[Research and Science S.L.]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S2529-850X2021000800006</article-id>
<article-id pub-id-type="doi">10.19230/jonnpr.4128</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Telómeros, telomerasa y envejecimiento. Una visita al Premio Nobel de Fisiología y Medicina de 2009]]></article-title>
<article-title xml:lang="en"><![CDATA[Telomeres, telomerase and aging. A visit to the 2009 Nobel Prize in Physiology and Medicine]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Soriano-Amador]]></surname>
<given-names><![CDATA[Cristina]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Sánchez-Muniz]]></surname>
<given-names><![CDATA[Francisco J]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
<xref ref-type="aff" rid="Ab"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Complutense de Madrid  ]]></institution>
<addr-line><![CDATA[Madrid ]]></addr-line>
<country>España</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Universidad Complutense de Madrid Facultad de Farmacia ]]></institution>
<addr-line><![CDATA[Madrid ]]></addr-line>
<country>España</country>
</aff>
<aff id="A2b">
<institution><![CDATA[,Real Academia Nacional de Farmacia  ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>España</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>00</month>
<year>2021</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>00</month>
<year>2021</year>
</pub-date>
<volume>6</volume>
<numero>8</numero>
<fpage>1079</fpage>
<lpage>1100</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://scielo.isciii.es/scielo.php?script=sci_arttext&amp;pid=S2529-850X2021000800006&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.isciii.es/scielo.php?script=sci_abstract&amp;pid=S2529-850X2021000800006&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.isciii.es/scielo.php?script=sci_pdf&amp;pid=S2529-850X2021000800006&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen  Introducción. En octubre de 2009, Elizabeth H. Blackburn, Carol W. Greider y Jack W. Szostak fueron galardonados por sus descubrimientos sobre los telómeros y la enzima telomerasa con el Premio Nobel de Fisiología y Medicina. Posteriormente muchas investigaciones, entre las que destacan la de científicos españoles han demostrado el papel de los telómeros en el envejecimiento y en algunas patologías relacionadas.  Métodos. Para la realización de este trabajo se ha revisado tres aspectos: a) la información dada por el Comité del Nobel sobre las investigaciones de los tres galardonados; b) los mecanismos moleculares implicados en el proceso de protección de los telómeros por la acción de la telomerasa y c) la relación entre envejecimiento y sistema telómeros/telomerasa.  Resultados. En las células eucariotas los telómeros constituyen el extremo terminal de los cromosomas, los cuales se acortan en cada división celular. Cuando el acortamiento es crítico, se induce daño persistente al ADN en estos extremos, senescencia, apoptosis y pérdidas de la capacidad regenerativa de los tejidos. Dada la imposibilidad de replicación completa de los telómeros por la ADN polimerasa después de cada división celular, la telomerasa, una ribonucloproteína retrotranscriptasa, actúa alargando los extremos de los cromosomas, utilizando como molde una porción de su propio ARN. Muchos factores determinan la longitud de los telómeros, sobresaliendo el acortamiento de los telómeros y la pérdida de actividad telomerásica. Además, existen multitud de factores que condicionan las diferencias entre edad fisiológica y edad cronológica.  Conclusión. Entre las muchas teorías sobre el envejecimiento sobresale la que relaciona el acortamiento de los telómeros con la senescencia. No obstante se requieren más estudios en los que se determine qué mecanismos epigenéticos y de otra índole condicionan la pérdida de actividad telomerásica y la longitud de los telómeros.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract  Introduction. In October 2009, Elizabeth H. Blackburn, Carol W. Greider, and Jack W. Szostak were awarded the Nobel Prize in Physiology and Medicine for their discoveries about telomeres and the enzyme telomerase. Subsequently, many investigations, including that of Spanish scientists, have demonstrated the role of telomeres in aging and in some very prevalent pathologies.  Methods. Three topics were reviewed to perform this article: a) the information given by the Nobel Committee on the research of the three winners of 2009 award; b) the molecular mechanisms involved in the protection process of telomeres by the telomerase enzyme; and c) the relationship between aging and the telomere/telomerase system.  Results. In eukaryotic cells, telomeres constitute the terminal end of chromosomes, which are shortened within each cell division. When the shortening becomes critical, persistent DNA damage at these ends, senescence, apoptosis and loss of the tissues regenerative capacity are induced. Given the unfeasibility of telomeres complete replication by the DNA polymerase after each cell division, the telomerase, a reverse transcriptase ribonucloprotein, works by lengthening the ends of chromosomes, using as a template a portion of its own RNA. Several factors determine the length of telomeres and/or the loss of telomerase activity, with aging standing out. In addition, there are many factors that determine the differences between physiological and chronological age.  Conclusion. Among aging theories, the one relating the shortening of telomeres with senescence stands out. However, more studies are required to determine which epigenetic and other mechanisms determine the loss of telomerase activity and the length of telomeres.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Disquerina]]></kwd>
<kwd lng="es"><![CDATA[Premio Nobel]]></kwd>
<kwd lng="es"><![CDATA[Shelterina]]></kwd>
<kwd lng="es"><![CDATA[Telómeros]]></kwd>
<kwd lng="es"><![CDATA[telomerasa]]></kwd>
<kwd lng="es"><![CDATA[telosoma]]></kwd>
<kwd lng="en"><![CDATA[Aging]]></kwd>
<kwd lng="en"><![CDATA[dyskerin]]></kwd>
<kwd lng="en"><![CDATA[Nobel prize]]></kwd>
<kwd lng="en"><![CDATA[shelterin]]></kwd>
<kwd lng="en"><![CDATA[telomeres]]></kwd>
<kwd lng="en"><![CDATA[telomerase]]></kwd>
</kwd-group>
</article-meta>
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