Publications by authors named "E Balsa"

Article Synopsis
  • Deficiencies in the electron transport chain (ETC) contribute to mitochondrial diseases, but the reasons for different cellular sensitivities to this disruption are not fully understood.
  • This study finds that under ETC inhibition, a different type of tricarboxylic acid (TCA) cycle is activated to maintain malate levels and produce NADPH, which is crucial for cell function.
  • The research highlights how astrocytes, which express specific enzymes like Pyruvate carboxylase (PC) and ME1 more than neurons, demonstrate greater resilience to ETC issues, suggesting potential therapeutic strategies for managing mitochondrial diseases.
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The brain is a highly metabolic organ, composed of multiple cell classes, that controls crucial functions of the body. Although neurons have traditionally been the main protagonist, astrocytes have gained significant attention over the last decade. In this regard, astrocytes are a type of glial cells that have recently emerged as critical regulators of central nervous system (CNS) function and play a significant role in maintaining brain energy metabolism.

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Dendritic cells (DCs) have a role in the development and activation of self-reactive pathogenic T cells. Genetic variants that are associated with the function of DCs have been linked to autoimmune disorders, and DCs are therefore attractive therapeutic targets for such diseases. However, developing DC-targeted therapies for autoimmunity requires identification of the mechanisms that regulate DC function.

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Dendritic cells (DCs) control the generation of self-reactive pathogenic T cells. Thus, DCs are considered attractive therapeutic targets for autoimmune diseases. Using single-cell and bulk transcriptional and metabolic analyses in combination with cell-specific gene perturbation studies we identified a negative feedback regulatory pathway that operates in DCs to limit immunopathology.

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Chronic obstructive pulmonary disease (COPD), whose main risk factor is cigarette smoking (CS), is one of the most common diseases globally. Some COPD patients also develop pulmonary hypertension (PH), a severe complication that leads to premature death. Evidence suggests reactive oxygen species (ROS) involvement in COPD and PH, especially regarding pulmonary artery smooth muscle cells (PASMC) dysfunction.

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