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Astrocyte activation and reactive gliosis-A new target in stroke?
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- Pekny, Milos, 1965 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience
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- Wilhelmsson, Ulrika, 1970 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience
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- Tatlisumak, Turgut (author)
- Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience
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- (creator_code:org_t)
- Elsevier BV, 2019
- 2019
- English.
- In: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 689, s. 45-55
- Journal article (peer-reviewed)
Abstract
Subject headings
Close
- Stroke is an acute insult to the central nervous system (CNS) that triggers a sequence of responses in the acute, subacute as well as later stages, with prominent involvement of astrocytes. Astrocyte activation and reactive gliosis in the acute stage of stroke limit the tissue damage and contribute to the restoration of homeostasis. Astrocytes also control many aspects of neural plasticity that is the basis for functional recovery. Here, we discuss the concept of intermediate filaments (nanofilaments) and the complement system as two handles on the astrocyte responses to injury that both present attractive opportunities for novel treatment strategies modulating astrocyte functions and reactive gliosis.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Neurovetenskaper (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Neurosciences (hsv//eng)
Keyword
- Astrocytes
- Reactive gliosis
- Intermediate filaments (Nanofilaments)
- GFAP
- Vimentin
- Nestin
- Stroke
- fibrillary acidic protein
- complement peptide c3a
- promotes functional
- recovery
- regulatory volume decrease
- focal cerebral-ischemia
- intermediate-filaments
- mice deficient
- chondroitinase abc
- neural
- plasticity
- cell-volume
Publication and Content Type
- ref (subject category)
- art (subject category)
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