Linked Life Data

9316214

Source:http://linkedlifedata.com/resource/pubmed/id/9316214

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1997-11-18
pubmed:abstractText
A large body of data has now implicated elevations in the cytokine transforming growth factor-beta (TGF-beta) as a key mediator of tissue fibrosis. A number of mechanisms by which TGF-beta can be increased have been identified. Among them is the potent vasoconstrictor angiotensin II (ANG II). In vitro data indicate that ANG II, independent of blood pressure, increases synthesis and decreases degradation of pathological extracellular matrix components. These effects are largely, but not completely, mediated by ANG II induction of TGF-beta. In many models of renal fibrosis and in a number of human renal diseases, blockade of ANG II retards disease progression. Very recent studies indicate that ANG II blockade suppresses TGF-beta, whether the therapeutic agent is an angiotensin converting enzyme inhibitor or an ANG II type 1 receptor antagonist. These data suggest that an important antifibrotic, therapeutic effect of ANG II blockade is reduction of TGF-beta overexpression and raise the question of whether disease progression could be further retarded if ANG II blockade were optimized for maximal TGF-beta reduction rather than for normalization of systemic blood pressure.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0270-9295
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
455-66
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Angiotensin II in renal fibrosis: should TGF-beta rather than blood pressure be the therapeutic target?
pubmed:affiliation
Division of Nephrology, University of Utah School of Medicine, Salt Lake City 84132, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review