Literature DB >> 15846807

Role of glial cells in cerebral ischemia.

Maiken Nedergaard1, Ulrich Dirnagl1.   

Abstract

Despite intense efforts at the bench and at the bedside, few therapeutic strategies exist to combat the consequences of cerebral ischemia. Traditionally, a "neurocentric" view has dominated research in this field. Evidence is now accumulating that glial cells, in particular astrocytes, play an active and important role in the pathophysiology of cerebral ischemia. Brain energetics, water and ion homeostasis, inflammation, trophic factor production, vascular regulation, neuroneogenesis, and vasculogenesis, among others, are all under the control of glial cells. As a consequence, glial cells have been identified as promising targets for novel therapeutic approaches in brain protection. This review aims at dissecting possible protective as well as destructive roles of astrocytes (and other glial cells) in cerebral ischemia. By emphasizing open issues in this field, we hope to stimulate further research into this relatively unexplored aspect of brain pathophysiology. Copyright 2005 Wiley-Liss, Inc.

Entities:  

Mesh:

Year:  2005        PMID: 15846807     DOI: 10.1002/glia.20205

Source DB:  PubMed          Journal:  Glia        ISSN: 0894-1491            Impact factor:   8.073


  106 in total

1.  Astrocyte targeted overexpression of Hsp72 or SOD2 reduces neuronal vulnerability to forebrain ischemia.

Authors:  Lijun Xu; John F Emery; Yi-Bing Ouyang; Ludmila A Voloboueva; Rona G Giffard
Journal:  Glia       Date:  2010-07       Impact factor: 7.452

2.  Protective effect of carbamazepine on kainic acid-induced neuronal cell death through activation of signal transducer and activator of transcription-3.

Authors:  Hae Jeong Park; Su Kang Kim; Joo-Ho Chung; Jong Woo Kim
Journal:  J Mol Neurosci       Date:  2012-07-08       Impact factor: 3.444

3.  Gliotoxin-induced swelling of astrocytes hinders diffusion in brain extracellular space via formation of dead-space microdomains.

Authors:  Ang Doma Sherpa; Paula van de Nes; Fanrong Xiao; Jeremy Weedon; Sabina Hrabetova
Journal:  Glia       Date:  2014-03-31       Impact factor: 7.452

Review 4.  Neuroprotection for ischemic stroke: past, present and future.

Authors:  Myron D Ginsberg
Journal:  Neuropharmacology       Date:  2008-03-04       Impact factor: 5.250

Review 5.  Purinoceptors on neuroglia.

Authors:  Alexei Verkhratsky; Alexei Verkhrasky; Oleg A Krishtal; Geoffrey Burnstock
Journal:  Mol Neurobiol       Date:  2009-03-13       Impact factor: 5.590

6.  Nanomicellar formulation of coenzyme Q10 (Ubisol-Q10) effectively blocks ongoing neurodegeneration in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model: potential use as an adjuvant treatment in Parkinson's disease.

Authors:  Marianna Sikorska; Patricia Lanthier; Harvey Miller; Melissa Beyers; Caroline Sodja; Bogdan Zurakowski; Sandhya Gangaraju; Siyaram Pandey; Jagdeep K Sandhu
Journal:  Neurobiol Aging       Date:  2014-04-02       Impact factor: 4.673

7.  P2Y1R-initiated, IP3R-dependent stimulation of astrocyte mitochondrial metabolism reduces and partially reverses ischemic neuronal damage in mouse.

Authors:  Wei Zheng; Lora Talley Watts; Deborah M Holstein; Jimmy Wewer; James D Lechleiter
Journal:  J Cereb Blood Flow Metab       Date:  2013-01-16       Impact factor: 6.200

Review 8.  Neuroimmune Response in Ischemic Preconditioning.

Authors:  Ashley McDonough; Jonathan R Weinstein
Journal:  Neurotherapeutics       Date:  2016-10       Impact factor: 7.620

9.  Overexpression of human S100B exacerbates brain damage and periinfarct gliosis after permanent focal ischemia.

Authors:  Takashi Mori; Jun Tan; Gary W Arendash; Naoki Koyama; Yoshiko Nojima; Terrence Town
Journal:  Stroke       Date:  2008-05-01       Impact factor: 7.914

Review 10.  Role of signal transducer and activator of transcription 3 in neuronal survival and regeneration.

Authors:  Suzan Dziennis; Nabil J Alkayed
Journal:  Rev Neurosci       Date:  2008       Impact factor: 4.353

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.