作者: Yeri Kim , Joanne O. Davidson , Katherine C. Gunn , Anthony R. Phillips , Colin R. Green
DOI: 10.1016/BS.APCSB.2015.12.001
关键词:
摘要: Neurodegenerative, cardiovascular, and metabolic disorders, once triggered, share a number of common features, including sustained inflammatory cell activation vascular disruption. These shared pathways are induced independently any genetic predisposition to the disease or precise external stimulus. Glial cells respond injury with an innate immune response that includes release proinflammatory cytokines chemokines. Vascular endothelial may also be affected, leading opening blood-brain barrier facilitates invasion by circulating cells. Inflammation can trigger acute neural followed chronic inflammation plays key role in neurodegenerative conditions. Gap junction channels normally allow direct cell-to-cell communication. They formed docking two hemichannels, one contributed each neighboring While probability these is tightly controlled under resting conditions, hemichannels open factors, forming large, relatively nonselective membrane pore. In this review, we consider CNS system from perspective modulating connexin hemichannel prevent tissue damage arising excessive uncontrolled inflammation. We discuss channel roles microglia, astrocytes, both particular describe inflammasome pathway where they contribute its spread Finally, benefits block animal models brain injury.