Mitochondrial Reactive Oxygen Species and Type 1 Diabetes

摘要

Significance: The complex etiology of type 1 diabetes (T1D) is the outcome of failures in regulating immunity in combination with beta cell perturbations. Mitochondrial dysfunction in beta cells and immune cells may be involved in T1D pathogenesis. Mitochondrial energy production is essential for the major task of beta cells (the secretion of insulin in response to glucose). Mitochondria are a major site of reactive oxygen species (ROS) production. Under immune attack, mitochondrial ROS (mtROS) participate in beta cell damage. Similarly, T cell fate during immune responses is tightly regulated by mitochondrial physiology, morphology, and metabolism. Production of mtROS is essential for signaling in antigen-specific T cell activation. Mitochondrial dysfunction in T cells has been noted as a feature of some human autoimmune diseases.