Document Detail


Triggers and mediators of hemorrhagic transformation in cerebral ischemia.
MedLine Citation:
PMID:  14709787     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Intracerebral hemorrhagic transformation is a multifactorial phenomenon in which ischemic brain tissue converts into a hemorrhagic lesion with blood-vessel leakage, extravasation, and further brain injury. It has been estimated that up to 30-40% of all ischemic strokes undergo spontaneous hemorrhagic transformation, and this phenomenon may become even more prevalent with the increasing use of thrombolytic stroke therapy. An emerging conceptual model suggests that the loss of microvascular integrity and disruption of neurovascular homeostasis connects the experimental findings of blood-cell extravasation to brain injury after hemorrhage. In this short article, we examine mechanisms related to reperfusion injury and oxidative stress, leukocyte infiltration, vascular activation, and dysregulated extracellular proteolysis as potential triggers of hemorrhagic transformation. Perturbations in cell-cell and cell-matrix signaling within the hypothesized neurovascular unit may ultimately lead to neuroinflammation and apoptotic-like cell death in the parenchyma. Further investigations into the molecular mediators of hemorrhagic transformation may reveal new therapeutic targets for this clinically complex problem.
Authors:
Xiaoying Wang; Eng H Lo
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Molecular neurobiology     Volume:  28     ISSN:  0893-7648     ISO Abbreviation:  Mol. Neurobiol.     Publication Date:  2003 Dec 
Date Detail:
Created Date:  2004-01-07     Completed Date:  2004-03-09     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8900963     Medline TA:  Mol Neurobiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  229-44     Citation Subset:  IM    
Affiliation:
Neuroprotection Research Laboratory, Departments of Neurology and Radiology, Massachusetts General Hospital, Boston, MA. Wangxi@helix.mgh.harvard.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / physiology
Blood-Brain Barrier / physiology
Brain Ischemia / complications*,  physiopathology*
Cerebral Hemorrhage / etiology*,  physiopathology*
Extracellular Fluid / metabolism
Humans
Inflammation Mediators / metabolism
Microcirculation / metabolism,  pathology,  physiopathology
Reperfusion Injury / etiology,  physiopathology
Grant Support
ID/Acronym/Agency:
P50 NS 10828/NS/NINDS NIH HHS; R01 NS 37074/NS/NINDS NIH HHS; R01 NS 40529/NS/NINDS NIH HHS; R02 NS 38731/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Inflammation Mediators

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


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