Astrogliosis

被引:500
作者
Sofroniew, Michael V. [1 ]
机构
[1] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurobiol, Los Angeles, CA 90095 USA
来源
COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY | 2015年 / 7卷 / 02期
基金
美国国家卫生研究院;
关键词
SPINAL-CORD-INJURY; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; NERVOUS-SYSTEM INFLAMMATION; REACTIVE ASTROCYTES; NEURODEGENERATIVE DISEASE; NEURONAL DYSFUNCTION; MULTIPLE-SCLEROSIS; ALEXANDER-DISEASE; GLUTAMATE RELEASE; TRANSGENIC MICE;
D O I
10.1101/cshperspect.a020420
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
In addition to their many functions in the healthy central nervous system (CNS), astrocytes respond to CNS damage and disease through a process called astrogliosis. For many decades, astrogliosis was sparsely studied and enigmatic. This article examines recent evidence supporting a definition of astrogliosis as a spectrum of heterogeneous potential changes in astrocytes that occur in a context-specific manner as determined by diverse signaling events that vary with the nature and severity of different CNS insults. Astrogliosis is associated with essential beneficial functions, but under specific circumstances can lead to harmful effects. Potential dysfunctions of astrocytes and astrogliosis are being identified that can contribute to, or be primary causes of, CNS disorders, leading to the notion of astrocytopathies. A conceptual framework is presented that allows consideration of normally occurring and dysfunctional astrogliosis and their different roles in CNS disorders.
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页数:16
相关论文
共 104 条
  • [61] Martin JL, 2013, CURR DRUG TARGETS, V14, P1308
  • [62] Spinal cord injury reveals multilineage differentiation of ependymal cells
    Meletis, Konstantinos
    Barnabe-Heider, Fanie
    Carlen, Marie
    Evergren, Emma
    Tomilin, Nikolay
    Shupliakov, Oleg
    Frisen, Jonas
    [J]. PLOS BIOLOGY, 2008, 6 (07) : 1494 - 1507
  • [63] Messing A, 1998, AM J PATHOL, V152, P391
  • [64] Alexander Disease
    Messing, Albee
    Brenner, Michael
    Feany, Mel B.
    Nedergaard, Maiken
    Goldman, James E.
    [J]. JOURNAL OF NEUROSCIENCE, 2012, 32 (15) : 5017 - 5023
  • [65] GFAP in health and disease
    Middeldorp, J.
    Hol, E. M.
    [J]. PROGRESS IN NEUROBIOLOGY, 2011, 93 (03) : 421 - 443
  • [66] Depression, cytokines, and glial function
    Miller, DB
    O'Callaghan, JP
    [J]. METABOLISM-CLINICAL AND EXPERIMENTAL, 2005, 54 (05): : 33 - 38
  • [67] Essential protective roles of reactive astrocytes in traumatic brain injury
    Myer, D. J.
    Gurkoff, G. G.
    Lee, S. M.
    Hovda, D. A.
    Sofroniew, M. V.
    [J]. BRAIN, 2006, 129 : 2761 - 2772
  • [68] Astrocytes expressing ALS-linked mutated SOD1 release factors selectively toxic to motor neurons
    Nagai, Makiko
    Re, Diane B.
    Nagata, Tetsuya
    Chalazonitis, Alcmene
    Jessell, Thomas M.
    Wichterle, Hynek
    Przedborski, Serge
    [J]. NATURE NEUROSCIENCE, 2007, 10 (05) : 615 - 622
  • [69] Mice lacking GFAP are hypersensitive to traumatic cerebrospinal injury
    Nawashiro, H
    Messing, A
    Azzam, N
    Brenner, M
    [J]. NEUROREPORT, 1998, 9 (08) : 1691 - 1696
  • [70] Conditional ablation of Stat3 or Socs3 discloses a dual role for reactive astrocytes after spinal cord injury
    Seiji Okada
    Masaya Nakamura
    Hiroyuki Katoh
    Tamaki Miyao
    Takuya Shimazaki
    Ken Ishii
    Junichi Yamane
    Akihiko Yoshimura
    Yukihide Iwamoto
    Yoshiaki Toyama
    Hideyuki Okano
    [J]. Nature Medicine, 2006, 12 (7) : 829 - 834