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  • Author: Federico V. Pallardó x
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Jesús Beltrán-García Center for Biomedical Research Network on Rare Diseases (CIBERER), Instituto de Salud Carlos III, Valencia, Spain
Biomedical Research Institute INCLIVA, Valencia, Spain
Department of Physiology, Medicine and Dentistry School, University of Valencia, Valencia, Spain

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Rebeca Osca-Verdegal Center for Biomedical Research Network on Rare Diseases (CIBERER), Instituto de Salud Carlos III, Valencia, Spain
Biomedical Research Institute INCLIVA, Valencia, Spain
Department of Physiology, Medicine and Dentistry School, University of Valencia, Valencia, Spain

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José Luis García-Giménez Center for Biomedical Research Network on Rare Diseases (CIBERER), Instituto de Salud Carlos III, Valencia, Spain
Biomedical Research Institute INCLIVA, Valencia, Spain
Department of Physiology, Medicine and Dentistry School, University of Valencia, Valencia, Spain

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Federico V. Pallardó Center for Biomedical Research Network on Rare Diseases (CIBERER), Instituto de Salud Carlos III, Valencia, Spain
Biomedical Research Institute INCLIVA, Valencia, Spain
Department of Physiology, Medicine and Dentistry School, University of Valencia, Valencia, Spain

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Oxidative stress is an important contributor to sepsis and one of the most important causes of death in intensive care units. Even though sepsis pathogenesis remains obscure due to its heterogenicity and complexity, there is increasing evidence that oxidants and antioxidants play a key role in its onset and progression. Recent evidence suggests that pyroptosis is required for defense against bacterial infection, and it is active in several cell types during sepsis. One of the most relevant mediators of pyroptosis is the NLRP3 inflammasome, and the oxidative stress/NLRP3 signaling pathway is one of the main upstream signals involved in its activation. So, it is of special relevance to clarify how oxidative stress and antioxidants can modulate pyroptosis signals and therefore decrease the deleterious effects that both oxidative stress and pyroptosis-related cytokines can induce in the tissues during sepsis. Recent studies evaluating several antioxidants are promising, but further trials are needed to confirm their potential role as agents to block NLRP3 and mitigate the exacerbated inflammasome-related responses during sepsis.

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Davinia Domínguez-González Department of Physiology, Faculty of Medicine and Dentistry, University of Valencia- INCLIVA, Valencia, Spain

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Blanca Romero-Llopis Department of Physiology, Faculty of Medicine and Dentistry, University of Valencia- INCLIVA, Valencia, Spain

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Marta Roldán-Lázaro Department of Physiology, Faculty of Medicine and Dentistry, University of Valencia- INCLIVA, Valencia, Spain
Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Valencia, Spain

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Lorena Baquero Department of Physiology, Faculty of Medicine and Dentistry, University of Valencia- INCLIVA, Valencia, Spain
Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Valencia, Spain

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Rita Noverques Department of Physiology, Faculty of Medicine and Dentistry, University of Valencia- INCLIVA, Valencia, Spain

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Federico V Pallardó Department of Physiology, Faculty of Medicine and Dentistry, University of Valencia- INCLIVA, Valencia, Spain
Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Valencia, Spain

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Juan Antonio Navarro Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Valencia, Spain
Department of Genetics, Universitat de València, Valencia, Spain
INCLIVA Biomedical Research Institute, Unversitat de València, Valencia, Spain

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Pilar Gonzalez-Cabo Department of Physiology, Faculty of Medicine and Dentistry, University of Valencia- INCLIVA, Valencia, Spain
Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Valencia, Spain

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l-glutamate is one of the major neurotransmitters in the central nervous system, directly and indirectly involved in numerous brain functions. In several neurodegenerative diseases, it has been observed that an excess of extracellular glutamate overstimulates glutamate receptors, leading to exacerbated neuronal excitation in a process of excitotoxicity and oxidative damage that promotes neuronal death. A number of l-glutamate transporters have been identified in the membrane of neurons and astrocytes. They are responsible for the reuptake of glutamate released into the synaptic cleft after excitatory neurotransmission concomitantly regulating the extracellular concentration of glutamate, protecting neurons from its excitotoxic action. Among all of them, literature highlights glutamate transporter 1, known as excitatory amino acid transporter type 2 in humans and glutamate transporter type 1 in rodents, also known as solute carrier family 1 member 2. It is the predominant glutamate transporter in the brain and ensures the majority of l-glutamate reuptake. Decreased expression of this transporter along with increased levels of oxidative stress have been observed in several chronic and acute neurodegenerative disorders. For this reason, the use of drugs capable of both increasing the expression of glutamate transporter 1 and mitigating oxidative damage has been proposed as an effective therapeutic strategy for these pathologies. We present in this work an overview of the main drugs displaying such a double effect.

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