Linked Life Data

16875736

Source:http://linkedlifedata.com/resource/pubmed/id/16875736

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-3
pubmed:dateCreated
2006-11-2
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0161-5890
pubmed:author
pubmed:issnType
Print
pubmed:volume
44
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
95-102
pubmed:dateRevised
2008-7-9
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Complement-related molecular events in sepsis leading to heart failure.
pubmed:affiliation
Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Extramural