Linked Life Data

16495897

Source:http://linkedlifedata.com/resource/pubmed/id/16495897

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-2-23
pubmed:abstractText
Liver fibrosis is the end result of an imbalance between synthesis and degradation of extracellular matrix proteins of the liver. The extracellular matrix of the liver is complex. It comprises multiple components of three major types of macromolecules: proteins, glycoproteins and proteoglycans. The normal liver contains limited amounts of extracellular matrix composed of elastin, fibronectin, collagen, proteoglycans and other macromolecules. These molecules have specific structure-function properties. In the liver they provide a structural framework and modulate tissue repair. The fibrogenesis is a reaction to liver injury, it leads to marked impairment of hepatic sinusoidal blood flow and ultimately to cirrhosis associated with portal hypertension and hepatocyte dysfunction. The process of fibrosis is the result from complex interactions between extracellular matrix macromolecules, hepatic cells, cytokines and growth factors, that activate the stellate cells of the liver to induce the synthesis of extracellular matrix components that deposit into the local extracellular matrix and to produce the inhibitor of metalloproteinase. The end result of these activities is an imbalance in the synthesis/degradation homeostasis of the liver, that is, liver fibrosis.
pubmed:language
ita
pubmed:journal
pubmed:status
PubMed-not-MEDLINE
pubmed:month
Sep
pubmed:issn
1121-421X
pubmed:author
pubmed:issnType
Print
pubmed:volume
44
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
149-58
pubmed:dateRevised
2006-11-15
pubmed:year
1998
pubmed:articleTitle
[The physiopathological mechanism of hepatic fibrosis].
pubmed:affiliation
Dipartimento di Gastroenterologia, Università degli Studi di Roma La Sapienza, Rome.
pubmed:publicationType
Journal Article, English Abstract