Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2010-12-16
pubmed:abstractText
Activation of the intra-renal renin-angiotensin system (RAS) and the subsequent generation of angiotensin II (Ang II) are important mediators of haemodynamic changes in both health and disease. However, the effects of locally produced Ang II are not limited to haemodynamic actions. Ang II is also an important stimulus for tubular hypertrophy with the induction of growth factors, including transforming growth factor (TGF)-?(1) and connective tissue growth factor. In this article, we explore the direct pro-fibrotic effects of Ang II and its role in inducing tubular epithelial to mesenchymal transition (EMT, also known as type 2 EMT), a known mediator of renal fibrogenesis. There is accumulating evidence that Ang II is able to induce EMT by both TGF-dependent and TGF-independent actions, both in vitro and in vivo. Moreover, blockade of the RAS has synergistic renoprotective effects across a number of causally different forms of renal disease. There is hope that targeted combinations to offset angiotensin-converting enzyme escape in the setting of RAS blockade will eventually achieve the long-term efficacy that has been expected for so long.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1422-6421
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 S. Karger AG, Basel.
pubmed:issnType
Electronic
pubmed:volume
193
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
74-84
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Angiotensin II and its role in tubular epithelial to mesenchymal transition associated with chronic kidney disease.
pubmed:affiliation
Danielle Alberti Memorial Centre for Diabetes Complications, Baker IDI Heart and Diabetes Institute, Melbourne, VIC, Australia. wendy.burns@bakeridi.edu.au
pubmed:publicationType
Journal Article, Review