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.