Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2007-6-14
pubmed:abstractText
The hepatotoxic effects of alcohol have been described in detail, but mechanisms underlying the hepatotoxicity have been only partially characterized. Recently, increasing lines of evidence indicate that Kupffer cells play multiple roles in initiation and progression of alcoholic steatohepatitis. After ethanol exposure, Kupffer cells are activated via a mechanism dependent on gut-derived endotoxin, and release active mediators such as proinflammatory cytokines and eicosanoids. These mediators are responsible for the pathophysiology of alcoholic steatohepatitis. This review discusses the current concept of Kupffer cell-mediated steatohepatitis and how it relates to the hypothesis on the mechanism by which alcoholic steatohepetitis is caused, as well as several key issues that have to be addressed in this field: (i) How do Kupffer cells undergo priming and activation during alcoholic steatohepatitis?; (ii) What kind of mediators are involved?; and (iii) How does the concept translate into a strategy for therapeutics of alcoholic steatohepatitis?
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0815-9319
pubmed:author
pubmed:issnType
Print
pubmed:volume
22 Suppl 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S59-61
pubmed:dateRevised
2010-6-9
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Anti-inflammatory strategies in alcoholic steatohepatitis.
pubmed:affiliation
Department of Gastroenterology, Juntendo University School of Medicine, Tokyo, Japan.
pubmed:publicationType
Journal Article, Review