Document Detail


What have genetically engineered mice taught us about ischemic injury?
MedLine Citation:
PMID:  15032714     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Stroke, is the third leading cause of death and disability in the Western world. Stroke refers to set of ischemic conditions resulting from the occlusion or hemorrhage of blood vessels supplying the brain. Loss of blood flow to the brain results in neuronal injury due to both oxygen and nutrient deprivation and the activation of injurious signal cascades. Ultimately cerebral ischemia results in death and dysfunction of brain cells, and neurological deficits that reflect the location and size of the compromised brain area. Injury due to ischemic stroke occurs by a highly choreographed series of complex spatial and temporal events that evolve over hours to days. These events involve complex interactions between fundamental cell injury mechanisms including excitotoxicity and ionic imbalance, oxidative and nitrosative stress, apoptotic-like cell death and inflammatory responses. Genetically engineered mice have been valuable tools to probe putative mechanisms of neuronal death and uncover potential strategies that might render neurons resistant to ischemic injury. Findings from experimental stroke studies in genetically engineered animals are discussed.
Authors:
Dong Liang; Ted M Dawson; Valina L Dawson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Current molecular medicine     Volume:  4     ISSN:  1566-5240     ISO Abbreviation:  Curr. Mol. Med.     Publication Date:  2004 Mar 
Date Detail:
Created Date:  2004-03-22     Completed Date:  2004-08-10     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  101093076     Medline TA:  Curr Mol Med     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  207-25     Citation Subset:  IM    
Affiliation:
Department of Neurology, Johns Hopkins University School of Medicine, 733 North Broadway Street, Suit 731, Baltimore, MD 21205, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis
Brain Injuries / pathology*
Brain Ischemia*
Cell Membrane / metabolism
Cell Nucleus / metabolism
Cloning, Molecular
Disease Models, Animal
Growth Substances / metabolism
Humans
Inflammation
Mice
Mice, Transgenic
Nitrogen / metabolism
Oxidative Stress
Signal Transduction
Grant Support
ID/Acronym/Agency:
NS39148/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Growth Substances; 7727-37-9/Nitrogen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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