<?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>0535-5133</journal-id>
<journal-title><![CDATA[Investigación Clínica]]></journal-title>
<abbrev-journal-title><![CDATA[Invest. clín]]></abbrev-journal-title>
<issn>0535-5133</issn>
<publisher>
<publisher-name><![CDATA[Instituto de Investigaciones Clínicas "Dr. Américo Negrette", Facultad de Medicina, Universidad del Zulia]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0535-51332024000200230</article-id>
<article-id pub-id-type="doi">10.54817/ic.v65n2a09</article-id>
<title-group>
<article-title xml:lang="en"><![CDATA[Mechanisms of programmed cell death: structural and functional pathways. A narrative review.]]></article-title>
<article-title xml:lang="es"><![CDATA[Mecanismos de muerte celular programada: vías estructurales y funcionales. Una revisión narrativa.]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Fernández-Lázaro]]></surname>
<given-names><![CDATA[Diego]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
<xref ref-type="aff" rid="A a"/>
<xref ref-type="aff" rid="A3"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Sanz]]></surname>
<given-names><![CDATA[Begoña]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Seco-Calvo]]></surname>
<given-names><![CDATA[Jesús]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
<xref ref-type="aff" rid="A a"/>
<xref ref-type="aff" rid="A6"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,University of Valladolid Faculty of Health Sciences Department of Cellular Biology, Genetics, Histology and Pharmacology]]></institution>
<addr-line><![CDATA[Soria ]]></addr-line>
<country>Spain</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,University of Valladolid Faculty of Medicine Neurobiology Research Group]]></institution>
<addr-line><![CDATA[Valladolid ]]></addr-line>
<country>Spain</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,SARCELLOMICS® Research Group  ]]></institution>
<addr-line><![CDATA[León ]]></addr-line>
<country>Spain</country>
</aff>
<aff id="Af4">
<institution><![CDATA[,University of the Basque Country Department of Physiology ]]></institution>
<addr-line><![CDATA[Leioa ]]></addr-line>
<country>Spain</country>
</aff>
<aff id="Af5">
<institution><![CDATA[,Biocruces Bizkaia Health Research Institute  ]]></institution>
<addr-line><![CDATA[Barakaldo ]]></addr-line>
<country>Spain</country>
</aff>
<aff id="Af6">
<institution><![CDATA[,University of León Institute of Biomedicine ]]></institution>
<addr-line><![CDATA[León ]]></addr-line>
<country>Spain</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>06</month>
<year>2024</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>06</month>
<year>2024</year>
</pub-date>
<volume>65</volume>
<numero>2</numero>
<fpage>230</fpage>
<lpage>252</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://ve.scielo.org/scielo.php?script=sci_arttext&amp;pid=S0535-51332024000200230&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://ve.scielo.org/scielo.php?script=sci_abstract&amp;pid=S0535-51332024000200230&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://ve.scielo.org/scielo.php?script=sci_pdf&amp;pid=S0535-51332024000200230&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Apoptosis, necroptosis, and autophagy are cellular mechanisms by which cells are programmed to die under various physiological and developmental stimuli. A multitude of protein mediators of programmed cell death have been identified, and apoptosis, necroptosis, and autophagy signals have been found to utilize common pathways that elucidate the proteins involved. This narrative review focuses on caspase-dependent and caspase-independent programmed cell death systems. Including studies of caspase-dependent programmed cell death, extrinsic pathway apoptotic mechanisms, phosphatidylserine (PS), FAS (APO-1/CD95), tumor necrosis factor (TNF) receptor type 1 (TNF-R1) and TNF-related apoptosis-inducing ligand (TRAIL), and intrinsic or mitochondrial pathway such as cytochrome C, the Bcl-2 family of proteins and Smac/Diablo. The Bcl-2 family has apoptotic mediators Bcl-2-associated X protein (Bax) and Bcl-2 homologous antagonist/killer (Bak), Bcl-2-interacting protein BIM (Bim), Bcl-2 agonist of cell death (Bad), Bid, Bcl-2 adenovirus E1B 19kDa-interacting protein 1 NIP3 (Bnip3), BMF, HRK, Noxa and PUMA and antiapoptotic proteins such as Bcl-2 itself, Mcl-1, Bcl-w, A1, and Bcl-XL. Moreover, caspase-independent programmed cell death pathways include the mitochondrial pathway with the protein mediators apoptosis inducing factor (AIF) and endonuclease G, and the pathways necroptosis, and autophagy. Understanding programmed cell death from those reported in this review could shed substantial light on the processes of biological homeostasis. In addition, identifying specific proteins involved in these processes is mandatory to identify molecular biomarkers and therapeutic targets. Furthermore, it could provide the ability to modulate the programmed cell death response and could lead to new therapeutic interventions in a disease.]]></p></abstract>
<abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen La apoptosis, la necroptosis y la autofagia son mecanismos celulares mediante los cuales las células se programan para morir bajo una amplia gama de estímulos fisiológicos. Esta revisión describe en los sistemas de muerte celular programada dependientes e independientes de la caspasa. Los estudios incluidos sobre la muerte celular programada dependiente de la caspasa incluyen mecanismos apoptóticos de la vía extrínseca que incluyen fosfatidilserina (PS), FAS (APO-1/CD95), receptor del factor de necrosis tumoral (FNT) tipo 1 (FNT-R1) e inductor de la apoptosis relacionada con ligando FNT (TRAIL) y vía intrínseca o mitocondrial como el citocromo C, la familia de proteínas Bcl-2 y Smac/Diablo. La familia Bcl-2 tiene mediadores apoptóticos, proteína X asociada a Bcl-2 (Bax) y antagonista/asesino homólogo de Bcl-2 (Bak), proteína BIM que interactúa con Bcl-2 (Bim), agonista de la muerte celular de Bcl-2 (Bad), Bid, proteína 1 que interactúa con el adenovirus E1B 19kDa de Bcl-2, NIP3 (Bnip3), BMF, HRK, Noxa y PUMA y proteínas antiapoptóticas como la propia Bcl-2, Mcl-1, Bcl-w, A1 y Bcl-XL. Además, las vías de muerte celular programada independientes de la caspasa incluyen la vía mitocondrial con los mediadores proteicos factor inductor de apoptosis (FIA) y endonucleasa G, las vías necroptosis y autofagia. Comprender la muerte celular programada a partir de los contenidos descritos en esta revisión podría arrojar luz sustancial sobre los procesos de la homeostasis biológica y podría proporcionar la capacidad de modular la respuesta de muerte celular programada y conducir a nuevas intervenciones terapéuticas en una amplia gama de enfermedades.]]></p></abstract>
<kwd-group>
<kwd lng="en"><![CDATA[apoptosis]]></kwd>
<kwd lng="en"><![CDATA[caspases]]></kwd>
<kwd lng="en"><![CDATA[mitochondrial/intrinsic pathway]]></kwd>
<kwd lng="en"><![CDATA[extrinsic pathway]]></kwd>
<kwd lng="en"><![CDATA[necroptosis]]></kwd>
<kwd lng="en"><![CDATA[autophagy]]></kwd>
<kwd lng="es"><![CDATA[apoptosis]]></kwd>
<kwd lng="es"><![CDATA[caspasas]]></kwd>
<kwd lng="es"><![CDATA[vía mitocondrial/intrínseca]]></kwd>
<kwd lng="es"><![CDATA[vía extrínseca]]></kwd>
<kwd lng="es"><![CDATA[necroptosis]]></kwd>
<kwd lng="es"><![CDATA[autofagia]]></kwd>
</kwd-group>
</article-meta>
</front><back>
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