Aberrant Calcium Signals in Reactive Astrocytes: A Key Process in Neurological Disorders
Astrocytes are abundant cells in the brain that regulate multiple aspects of neural tissue homeostasis by providing structural and metabolic support to neurons, maintaining synaptic environments and regulating blood flow. Recent evidence indicates that astrocytes also actively participate in brain f...
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Published in | International journal of molecular sciences Vol. 20; no. 4; p. 996 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
MDPI AG
25.02.2019
MDPI |
Subjects | |
Online Access | Get full text |
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Summary: | Astrocytes are abundant cells in the brain that regulate multiple aspects of neural tissue homeostasis by providing structural and metabolic support to neurons, maintaining synaptic environments and regulating blood flow. Recent evidence indicates that astrocytes also actively participate in brain functions and play a key role in brain disease by responding to neuronal activities and brain insults. Astrocytes become reactive in response to injury and inflammation, which is typically described as hypertrophy with increased expression of glial fibrillary acidic protein (GFAP). Reactive astrocytes are frequently found in many neurological disorders and are a hallmark of brain disease. Furthermore, reactive astrocytes may drive the initiation and progression of disease processes. Recent improvements in the methods to visualize the activity of reactive astrocytes in situ and in vivo have helped elucidate their functions. Ca
signals in reactive astrocytes are closely related to multiple aspects of disease and can be a good indicator of disease severity/state. In this review, we summarize recent findings concerning reactive astrocyte Ca
signals. We discuss the molecular mechanisms underlying aberrant Ca
signals in reactive astrocytes and the functional significance of aberrant Ca
signals in neurological disorders. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 1422-0067 1661-6596 1422-0067 |
DOI: | 10.3390/ijms20040996 |