Document Detail


The role of the chemokines in myocardial ischemia and reperfusion.
MedLine Citation:
PMID:  15320517     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Chemokines critically regulate basal and inflammatory leukocyte trafficking and may play a role in angiogenesis. This review summarizes our current understanding of the regulation and potential role of the chemokines in myocardial ischemia and reperfusion. Reperfused myocardial infarction is associated with an inflammatory response leading to leukocyte recruitment, healing and scar formation. Neutrophil chemoattractants, such as the CXC chemokine CXCL8/Interleukin (IL)-8, are upregulated in the infarcted area inducing polymorphonuclear leukocyte infiltration. In addition, mononuclear cell chemoattractants, such as the CC chemokine CCL2/Monocyte Chemoattractant Protein (MCP)-1, are expressed, leading to monocyte and lymphocyte recruitment in the ischemic area. However, chemokines may have additional effects in healing infarcts beyond their leukotactic properties. We have recently described a marked transient induction of the angiostatic CXC chemokine CXCL10/Interferon-gamma inducible Protein (IP)-10 in the infarct. Upregulation of angiostatic factors, such as IP-10, in the first few hours following injury may inhibit premature angiogenesis, until the infarct is debrided and appropriate supportive matrix is formed. Suppression of IP-10 synthesis during the healing phase may allow formation of the wound neovessels, a critical process for infarct healing. Chemokine expression is also noted after a single brief ischemic insult in the absence of myocardial infarction, suggesting a potential role for a chemokine-induced inflammatory response in noninfarctive ischemic cardiomyopathy. Unlike cytokines, which have pleiotropic effects, chemokines have more specific cellular targets. Understanding of their role in myocardial infarction may allow us to design specific therapeutic strategies aiming at optimizing cardiac repair and preventing ventricular remodeling.
Authors:
Nikolaos G Frangogiannis
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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 vascular pharmacology     Volume:  2     ISSN:  1570-1611     ISO Abbreviation:  Curr Vasc Pharmacol     Publication Date:  2004 Apr 
Date Detail:
Created Date:  2004-08-23     Completed Date:  2004-12-02     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  101157208     Medline TA:  Curr Vasc Pharmacol     Country:  United Arab Emirates    
Other Details:
Languages:  eng     Pagination:  163-74     Citation Subset:  IM    
Affiliation:
Section of Cardiovascular Sciences, The Methodist Hospital, DeBakey Heart Center, Baylor College of Medicine, Houston, TX 77030, USA. ngf@bcm.tmc.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiomyopathies / etiology,  metabolism*
Chemokines / metabolism*
Chemokines, CC / metabolism,  physiology
Humans
Inflammation / metabolism
Inflammation Mediators / physiology
Models, Biological
Myocardial Infarction / metabolism
Myocardial Ischemia / complications,  metabolism*
Myocardial Reperfusion*
Myocardial Reperfusion Injury / metabolism
Receptors, Chemokine / metabolism
Terminology as Topic
Grant Support
ID/Acronym/Agency:
HL-42550/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Chemokines; 0/Chemokines, CC; 0/Inflammation Mediators; 0/Receptors, Chemokine

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