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Astrocyte activation and reactive gliosis.

Journal article
Authors Milos Pekny
Michael Nilsson
Published in Glia
Volume 50
Issue 4
Pages 427-34
ISSN 0894-1491
Publication year 2005
Published at Institute of Medical Biochemistry
Pages 427-34
Language en
Links dx.doi.org/10.1002/glia.20207
Keywords Animals, Astrocytes, metabolism, pathology, Brain Injuries, metabolism, pathology, Gliosis, metabolism, pathology, Humans
Subject categories Clinical neurophysiology, Cell biology

Abstract

Astrocytes become activated (reactive) in response to many CNS pathologies, such as stroke, trauma, growth of a tumor, or neurodegenerative disease. The process of astrocyte activation remains rather enigmatic and results in so-called "reactive gliosis," a reaction with specific structural and functional characteristics. In stroke or in CNS trauma, the lesion itself, the ischemic environment, disrupted blood-brain barrier, the inflammatory response, as well as in metabolic, excitotoxic, and in some cases oxidative crises--all affect the extent and quality of reactive gliosis. The fact that astrocytes function as a syncytium of interconnected cells both in health and in disease, rather than as individual cells, adds yet another dimension to this picture. This review focuses on several aspects of astrocyte activation and reactive gliosis and discusses its possible roles in the CNS trauma and ischemia. Particular emphasis is placed on the lessons learnt from mouse genetic models in which the absence of intermediate filament proteins in astrocytes leads to attenuation of reactive gliosis with distinct pathophysiological and clinical consequences.

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