<?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>1665-1146</journal-id>
<journal-title><![CDATA[Boletín médico del Hospital Infantil de México]]></journal-title>
<abbrev-journal-title><![CDATA[Bol. Med. Hosp. Infant. Mex.]]></abbrev-journal-title>
<issn>1665-1146</issn>
<publisher>
<publisher-name><![CDATA[Instituto Nacional de Salud, Hospital Infantil de México Federico Gómez]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1665-11462021000600597</article-id>
<article-id pub-id-type="doi">10.24875/bmhim.20000323</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Síndrome de disfunción de órganos y adaptación mitocondrial en el paciente séptico]]></article-title>
<article-title xml:lang="en"><![CDATA[Organ dysfunction syndrome and mitochondrial adaptation in the septic patient]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Donoso-Fuentes]]></surname>
<given-names><![CDATA[Alejandro]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Arriagada-Santis]]></surname>
<given-names><![CDATA[Daniela]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Hospital Clínico Metropolitano Dra. Eloísa Díaz Insunza Centro de Responsabilidad del Niño Unidad de Paciente Crítico Pediátrico]]></institution>
<addr-line><![CDATA[Santiago ]]></addr-line>
<country>Chile</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>12</month>
<year>2021</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>12</month>
<year>2021</year>
</pub-date>
<volume>78</volume>
<numero>6</numero>
<fpage>597</fpage>
<lpage>611</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S1665-11462021000600597&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S1665-11462021000600597&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S1665-11462021000600597&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen Piedra angular para la sobrevida y la evolución de los organismos es su capacidad de mantener un adecuado balance energético, así como también que las células respondan y se adapten al estrés ambiental. Por ello, ante la presencia de diversos factores se origina una respuesta de protección celular mediante la activación de señalización dependiente de la función mitocondrial. Sin embargo, esta reacción, esencial para la supervivencia individual de las células, puede ser perjudicial para la función orgánica (adaptación inadecuada), transformando el estrecho equilibrio entre ambas en el eje patogénico de la disfunción orgánica y su eventual recuperación en el paciente séptico. Las alteraciones macrocirculatorias y microcirculatorias contribuyen, indudablemente, a la disfunción orgánica en la etapa precoz del choque séptico, mientras que la falla metabólica-bioenergética intrínseca (hipoxia citopática) perpetúa una función celular inadecuada. Por lo tanto, la disfunción mitocondrial es un proceso clave en la inducción del síndrome de disfunción multiorgánica en el paciente séptico. Este síndrome puede considerarse como un complejo fenómeno adaptativo hipometabólico ante un estímulo inflamatorio excesivo y prolongado, para lograr la regulación de la homeostasis energética y la preservación de la función de los órganos. En el futuro, debería producirse una transición entre las opciones terapéuticas actuales consensuadas, que se limitan al control del foco infeccioso y el soporte hemodinámico y vital, hacia una reanimación metabólica basada en las alteraciones moleculares y genéticas desencadenadas por la infección.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract The ability to maintain an adequate energy balance and to respond and adapt to environmental stress at the cellular level are cornerstones for the survival and evolution of organisms. Therefore, in the presence of various factors, a cellular protection response is triggered by activation of mitochondrial function-dependent signaling. However, this essential reaction for individual cell survival can be detrimental to organ function (maladaptation), transforming the close balance between the two into the pathogenetic axis of organ dysfunction and eventual recovery in septic patients. Macrocirculatory and microcirculatory disruption undoubtedly contributes to organ dysfunction in the early stage of septic shock, while intrinsic metabolic-bioenergetic failure (cytopathic hypoxia) perpetuates inadequate cellular function. Therefore, mitochondrial dysfunction is a key process in the induction of multiple organ dysfunction syndrome in the septic patient. This syndrome can be considered as a complex hypometabolic adaptive phenomenon in the face of excessive and prolonged inflammatory stimulus to achieve regulation of energy homeostasis and preservation of organ function. In the future, there should be a transition from the current consensus therapeutic options, which are limited to control of the infectious focus, hemodynamic and life support, to metabolic resuscitation based on the molecular and genetic alterations triggered by the infection.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Mitocondria]]></kwd>
<kwd lng="es"><![CDATA[Sepsis]]></kwd>
<kwd lng="es"><![CDATA[Síndrome de disfunción multiorgánica]]></kwd>
<kwd lng="es"><![CDATA[Adaptación metabólica]]></kwd>
<kwd lng="es"><![CDATA[Estrés oxidativo]]></kwd>
<kwd lng="en"><![CDATA[Mitochondria]]></kwd>
<kwd lng="en"><![CDATA[Sepsis]]></kwd>
<kwd lng="en"><![CDATA[Multiple organ failure]]></kwd>
<kwd lng="en"><![CDATA[Metabolic adaption]]></kwd>
<kwd lng="en"><![CDATA[Oxidative stress]]></kwd>
</kwd-group>
</article-meta>
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