Document Detail


Complement-related molecular events in sepsis leading to heart failure.
MedLine Citation:
PMID:  16875736     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Despite intensive ongoing research efforts, the mortality of patients with sepsis remains unacceptably high. A significant number of clinical trials have failed to produce sufficient therapeutic strategies despite showing promising results in animal models. So far, many studies have focused on deterioration of the humoral and cellular components of the immune system, the main cause of death in septic patients being multi-organ failure. However, not much is known about the effects of the complement system on parenchymal cells of organs such as the heart. Recently, septic cardiomyopathy has been recognized as one of the major complications during sepsis, often determining the clinical outcome. In this review, we describe molecular events which are thought to be related to cardiac dysfunction during sepsis. A special emphasis will be placed on the complement system, which generates powerful anaphylatoxins (such as C5a) and which has recently been associated with septic cardiomyopathy. Together with the impact on cardiac function of various cytokines we will provide a synopsis of the current knowledge regarding the pathophysiology underlying cardiac failure during sepsis with a special emphasis on C5a and C5aR.
Authors:
Laszlo M Hoesel; Andreas D Niederbichler; Peter A Ward
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2006-07-27
Journal Detail:
Title:  Molecular immunology     Volume:  44     ISSN:  0161-5890     ISO Abbreviation:  Mol. Immunol.     Publication Date:  2007 Jan 
Date Detail:
Created Date:  2006-11-02     Completed Date:  2007-01-04     Revised Date:  2008-07-09    
Medline Journal Info:
Nlm Unique ID:  7905289     Medline TA:  Mol Immunol     Country:  England    
Other Details:
Languages:  eng     Pagination:  95-102     Citation Subset:  IM    
Affiliation:
Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Complement System Proteins / physiology*
Cytokines / physiology
HMGB1 Protein / physiology
Heart / physiopathology
Heart Failure / etiology*
Humans
Inflammation / physiopathology
Macrophage Migration-Inhibitory Factors / physiology
Membrane Proteins / physiology
Nitric Oxide / physiology
Receptors, Complement / physiology
Sepsis / complications*
Grant Support
ID/Acronym/Agency:
GM-29507/GM/NIGMS NIH HHS; GM-61656/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/C5AR1 protein, human; 0/Cytokines; 0/HMGB1 Protein; 0/Macrophage Migration-Inhibitory Factors; 0/Membrane Proteins; 0/Receptors, Complement; 10102-43-9/Nitric Oxide; 9007-36-7/Complement System Proteins

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


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