Mithilesh Kumar Jha, Dong Ho Park, Hyun Kook, In-Kyu Lee, Won-Ha Lee and Kyoungho Suk Pages 387 - 402 ( 16 )
The central nervous system (CNS) shows dynamic immune and inflammatory responses to a variety of insults having crucial implications for reactive gliosis. Glial cells in the CNS serve not only as the source, but also as targets of proinflammatory mediators. Undoubtedly, these cells efficiently work towards the disposal of tissue debris and promotion of wound healing as well as tissue repair. However, these non-neuronal glial cells synthesize and release numerous inflammatory mediators, which can be detrimental to neurons, axons, myelin, and the glia themselves. While an acute insult is typically transient and unlikely to be detrimental to neuronal survival, chronic neuroinflammation is a long-standing and often self-perpetuating response, which persists even long after the initial injury or insult. It can serve as a point of origin for diverse neurological disorders including Alzheimer's disease. Accumulating evidence demonstrates the contribution of metabolic dysfunction and mitochondrial failure to the pathogenesis of neuroinflammatory and neurodegenerative diseases. Neurodegenerative conditions are also characterized by increased oxidative and endoplasmic reticulum stresses and autophagy defects. Furthermore, neuroinflammatory conditions are accompanied by an alteration in glial energy metabolism. Here, we comprehensively review the metabolic hallmarks of glia-mediated neuroinflammation and how the glial metabolic shift orchestrates the neuroinflammatory response and pathophysiology of diverse neurological disorders.
Astrocyte, CNS, neuron, inflammation, neuroinflammation, neurodegeneration, metabolism, mitochondria, microglia, oxidative stress.
, , , , , Department of Pharmacology, Kyungpook National University School of Medicine, Daegu, Republic of Korea.