Abstract
Hypoxia, which is a lowered physiological oxygen tension, is an important biological signal as well as a component of many diseases. In central nervous system, hypoxia is associated with brain injury following the ischemic stroke. Recent studies indicate that hypoxia may not only induce a direct neuronal damage, but it may also initiate inflammatory responses by activating microglia. Toxic inflammatory mediators produced by activated microglia under hypoxic conditions exacerbate the neuronal injury during cerebral ischemia. Pharmacological inhibition of hypoxic activation of microglia may prove to be neuroprotective against ischemic stroke.
Keywords: hypoxia, microglia, inflammation, apoptosis, neurodegeneration, neuronal injury, ischemia
Current Neuropharmacology
Title: Hypoxia as an Initiator of Neuroinflammation: Microglial Connections
Volume: 3 Issue: 2
Author(s): Jiyeon Ock, Hee-Jung Cho, Su Hyung Hong, In Kyeom Kim and Kyoungho Suk
Affiliation:
Keywords: hypoxia, microglia, inflammation, apoptosis, neurodegeneration, neuronal injury, ischemia
Abstract: Hypoxia, which is a lowered physiological oxygen tension, is an important biological signal as well as a component of many diseases. In central nervous system, hypoxia is associated with brain injury following the ischemic stroke. Recent studies indicate that hypoxia may not only induce a direct neuronal damage, but it may also initiate inflammatory responses by activating microglia. Toxic inflammatory mediators produced by activated microglia under hypoxic conditions exacerbate the neuronal injury during cerebral ischemia. Pharmacological inhibition of hypoxic activation of microglia may prove to be neuroprotective against ischemic stroke.
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Cite this article as:
Ock Jiyeon, Cho Hee-Jung, Hong Hyung Su, Kim Kyeom In and Suk Kyoungho, Hypoxia as an Initiator of Neuroinflammation: Microglial Connections, Current Neuropharmacology 2005; 3 (2) . https://dx.doi.org/10.2174/1570159053586681
| DOI https://dx.doi.org/10.2174/1570159053586681 |
Print ISSN 1570-159X |
| Publisher Name Bentham Science Publisher |
Online ISSN 1875-6190 |
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