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Adaptaciones mitocondriales en el síndrome de dificultad respiratoria aguda / Mitochondrial adaptations in acute respiratory distress syndrome
Resumen
Resumen
Las mitocondrias desempeñan un papel importante en el metabolismo energético de la célula debido a la función principal de producción de energía biológicamente disponible en forma de adenosín trifosfato (ATP), mediante procesos bioquímicos como la fosforilación oxidativa, la beta oxidación de ácidos grasos y el ciclo de Krebs. El síndrome de dificultad respiratoria aguda es una enfermedad pulmonar grave caracterizada por la aparición de infiltrados alveolares difusos, respuesta inmunológica desregulada y lesión alveolocapilar que limita el intercambio de gases. Las células alveolares mantienen una tensión de oxígeno del 5% y las mitocondrias consumen oxígeno a través de la enzima citocromo c oxidasa en la cadena de transporte de electrones, lo que permite la producción de ATP. La reducción en el consumo de oxígeno es crucial en el daño mitocondrial, ya que las mitocondrias son sensibles a la hipoxemia, lo cual afecta la transferencia de moléculas en la cadena de transporte de electrones que alteran el ciclo de Krebs. La hipoxia por hipoxemia afecta la fusión y la fisión mitocondrial, mientras que la OXPHOS se remodela, principalmente en el complejo I, para mantener la integridad mitocondrial. La falta de oxígeno activa los factores inducibles por hipoxia, lo cual genera estrés oxidativo, acidosis y daño celular; por tal motivo, esta revisión tiene como objetivo describir las adaptaciones mitocondriales en el síndrome de dificultad respiratoria aguda.
Abstract
Mitochondria play an important role in cell energy metabolism due to the main function of producing biologically available energy in the form of adenosine triphosphate (ATP), through biochemical processes such as oxidative phosphorylation, beta oxidation of fatty acids and the Krebs cycle. Acute respiratory distress syndrome is a severe lung disease characterized by the appearance of diffuse alveolar infiltrates, dysregulated immune response and alveolocapillary injury that limits gas exchange. Alveolar cells maintain an oxygen tension of 5% and mitochondria consume oxygen through the cytochrome c oxidase enzyme in the electron transport chain, allowing ATP production. The reduction in oxygen consumption is crucial in mitochondrial damage, as mitochondria are sensitive to hypoxemia, affecting the transfer of molecules in the electron transport chain that disrupt the Krebs cycle. Hypoxia due to hypoxemia affects mitochondrial fusion and fission, while OXPHOS remodels, mainly in complex I, to maintain mitochondrial integrity. Lack of oxygen activates hypoxia-inducible factors, generating oxidative stress, acidosis and cell damage; therefore, this review aims to describe mitochondrial adaptations in acute respiratory distress syndrome.
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DOI: https://doi.org/10.24875/10.5281/zenodo.10998887
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