Source:http://linkedlifedata.com/resource/pubmed/id/17567477
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
2007-6-14
|
pubmed:abstractText |
Recent studies have shown that the renin-angiotensin system (RAS) plays a pivotal role in liver fibrosis. An intrahepatic RAS is expressed in chronically damaged livers, and angiotensin-II (AT-II) reportedly stimulates contraction and proliferation of the activated hepatic stellate cells (Ac-HSC), and increases the transforming growth factor-beta (TGF-beta) expression through angiotensin type-I receptors (AT1-R). Some studies have demonstrated that the clinically used angiotensin-converting enzyme (ACE) inhibitor (ACE-I), and AT1-R blockers (ARB) significantly attenuated experimental liver fibrosis along with suppression of the Ac-HSC and hepatic TGF-beta expression. Angiotensin-II also stimulates the tissue inhibitor of metalloproteinases-1 (TIMP-1) in a dose- and time-dependent manner via protein kinase-C as an intracellular signaling cascade in the Ac-HSC, and these effects are completely suppressed by ARB. Combination treatment with low-dose interferon (IFN) and ACE-I exerts a stronger inhibitory effect than either single agent on its own. In humans it has been reported that ARB markedly improved the liver fibrosis score and TGF-beta expression in patients with chronic hepatitis C and non-alcoholic steatohepatitis. Serum fibrosis markers also significantly improved by treatment with low-dose IFN and ACE-I in patients with chronic hepatitis C, refractory to IFN monotherapy. Collectively, these data suggest that the interaction between AT-II and AT1-R plays a pivotal role in liver fibrosis development. Because both ACE-I and ARB are widely used in clinical practice without serious side-effects, these drugs in combination with IFN may provide a new strategy for antifibrosis therapy.
|
pubmed:commentsCorrections | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II Type 1 Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin-Converting Enzyme...,
http://linkedlifedata.com/resource/pubmed/chemical/Tissue Inhibitor of...,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor A
|
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 |
S93-5
|
pubmed:dateRevised |
2010-6-9
|
pubmed:meshHeading |
pubmed-meshheading:17567477-Angiotensin II Type 1 Receptor Blockers,
pubmed-meshheading:17567477-Angiotensin-Converting Enzyme Inhibitors,
pubmed-meshheading:17567477-Animals,
pubmed-meshheading:17567477-Liver Cirrhosis,
pubmed-meshheading:17567477-Renin-Angiotensin System,
pubmed-meshheading:17567477-Tissue Inhibitor of Metalloproteinases,
pubmed-meshheading:17567477-Vascular Endothelial Growth Factor A
|
pubmed:year |
2007
|
pubmed:articleTitle |
Blockade of renin-angiotensin system in antifibrotic therapy.
|
pubmed:affiliation |
Third Department of Internal Medicine, Nara Medical University, Nara, Japan. yoshijih@naramed-u.ac.jp
|
pubmed:publicationType |
Journal Article,
Review
|