<?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>0028-3746</journal-id>
<journal-title><![CDATA[Neumología y cirugía de tórax]]></journal-title>
<abbrev-journal-title><![CDATA[Neumol. cir. torax]]></abbrev-journal-title>
<issn>0028-3746</issn>
<publisher>
<publisher-name><![CDATA[Sociedad Mexicana de Neumología y Cirugía de Tórax; Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas; Sociedad Cubana de Neumología; Sociedad Paraguaya de Neumología; Sociedad Boliviana de Neumología.]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0028-37462016000300227</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[El papel de la autofagia en enfermedades pulmonares]]></article-title>
<article-title xml:lang="en"><![CDATA[The role of autophagy in pulmonary diseases]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Maciel-Herrerías]]></surname>
<given-names><![CDATA[Mariana]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Cabrera-Benítez]]></surname>
<given-names><![CDATA[Sandra]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Nacional Autónoma de México  ]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>Mexico</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>09</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>09</month>
<year>2016</year>
</pub-date>
<volume>75</volume>
<numero>3</numero>
<fpage>227</fpage>
<lpage>236</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S0028-37462016000300227&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S0028-37462016000300227&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S0028-37462016000300227&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen: La autofagia es un proceso fundamental de degradación intracelular de organelos y proteínas dañadas. La autofagia es también un mecanismo esencial para la adaptación al estrés, la supervivencia y la homeostasis celular. Paradójicamente, la autofagia también puede promover la muerte celular, pero cuándo y cómo la autofagia puede tener funciones pro o antiapoptóticas, es aún desconocido. La autofagia involucra el reclutamiento y la degradación de organelos dañados, agregados de proteínas, proteínas de larga vida y patógenos en vesículas de doble membrana llamadas autofagosomas, que luego se fusionan con los lisosomas para formar los autofagolisosomas (o autolisosomas). Alteraciones en la autofagia han sido implicadas en una amplia gama de trastornos, incluyendo enfermedades pulmonares. En esta revisión, se discute lo que al presente se sabe sobre el papel de la autofagia en el inicio y la progresión de diferentes trastornos pulmonares. Algunos estudios indican que la autofagia podría tener un papel deletéreo en la patogénesis de la enfermedad pulmonar obstructiva crónica y del asma. En otros trastornos como la fibrosis pulmonar idiopática y la fibrosis quística, la inhibición de la autofagia puede contribuir a la patogénesis.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract: Autophagy is a fundamental process of intracellular degradation of damaged organelles and proteins. Autophagy is also a crucial mechanism for adaptation to stress, survival and cellular homeostasis. Paradoxically, autophagy can also promote cell death, but when and how autophagy may have pro- or anti-apoptotic functions is still unknown. Autophagy involves the recruitment and degradation of damaged organelles, protein aggregates, long-lived proteins and pathogens, into double membrane vesicles called autophagosomes which then fuse with the lysosome to form autolysosomes. Alterations in autophagy have been implicated in a wide range of disorders including lung diseases. In this review, we discuss what is currently known about the role of autophagy in the initiation and progression of different pulmonary disorders. Some studies indicate that autophagy could have a deleterious role in the pathogenesis of chronic obstructive pulmonary disease and asthma. In other disorders, such as idiopathic pulmonary fibrosis and cystic fibrosis, impaired autophagy may contribute to pathogenesis.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Apoptosis]]></kwd>
<kwd lng="es"><![CDATA[asma]]></kwd>
<kwd lng="es"><![CDATA[autofagia]]></kwd>
<kwd lng="es"><![CDATA[homeostasis]]></kwd>
<kwd lng="es"><![CDATA[enfermedad pulmonar obstructiva crónica]]></kwd>
<kwd lng="es"><![CDATA[fibrosis pulmonar idiopática]]></kwd>
<kwd lng="es"><![CDATA[fibrosis quística]]></kwd>
<kwd lng="en"><![CDATA[Apoptosis]]></kwd>
<kwd lng="en"><![CDATA[asthma]]></kwd>
<kwd lng="en"><![CDATA[autophagy]]></kwd>
<kwd lng="en"><![CDATA[homeostasis]]></kwd>
<kwd lng="en"><![CDATA[chronic obstructive pulmonary disease]]></kwd>
<kwd lng="en"><![CDATA[idiopathic pulmonary fibrosis]]></kwd>
<kwd lng="en"><![CDATA[cystic fibrosis]]></kwd>
</kwd-group>
</article-meta>
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