Astrocytes in glaucomatous optic neuropathy

M. Rosario Hernandez*, Haixi Miao, Thomas Lukas

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapter

127 Scopus citations

Abstract

Glaucoma, the second most prevalent cause of blindness worldwide, is a degenerative disease characterized by loss of vision due to loss of retinal ganglion cells. There is no cure for glaucoma, but early intervention with drugs and/or surgery may slow or halt loss of vision. Increased intraocular pressure (IOP), age, and genetic background are the leading risk factors for glaucoma. Our laboratory and other investigators have provided evidence that astrocytes are the cells responsible for many pathological changes in the glaucomatous optic nerve head (ONH). Over several years, in vivo and in vitro techniques characterized the changes in quiescent astrocytes that lead to the reactive phenotype in glaucoma. Reactive astrocytes alter the homeostasis and integrity of the neural and connective tissues in the ONH of human and experimental glaucoma in monkeys. During the transition of quiescent astrocytes to the reactive phenotype altered astrocyte homeostatic functions such as cell-cell communication, migration, growth factor pathway activation, and responses to oxidative stress may impact pathological changes in POAG. Our data also suggests that the creation of a non-supportive environment for the survival of RGC axons through remodeling of the ONH by reactive astrocytes leads to progression of glaucomatous optic neuropathy.

Original languageEnglish (US)
Title of host publicationGlaucoma
Subtitle of host publicationAn Open Window to Neurodegeneration and Neuroprotection
EditorsCarlo Nucci, Luciano Cerulli, Neville Osborne, Giacinto Bagetta
Pages353-373
Number of pages21
DOIs
StatePublished - 2008

Publication series

NameProgress in Brain Research
Volume173
ISSN (Print)0079-6123

Keywords

  • astrocytes
  • extracellular matrix
  • glaucoma
  • growth factors
  • migration
  • optic nerve head
  • oxidative stress
  • signal transduction

ASJC Scopus subject areas

  • Neuroscience(all)

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