Angiotensin II and its role in tubular epithelial to mesenchymal transition associated with chronic kidney disease

W. C. Burns, M. C. Thomas

Research output: Contribution to journalArticleResearchpeer-review

27 Citations (Scopus)

Abstract

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)-β 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.

Original languageEnglish
Pages (from-to)74-84
Number of pages11
JournalCells Tissues Organs
Volume193
Issue number1-2
DOIs
Publication statusPublished - 1 Dec 2010
Externally publishedYes

Keywords

  • Angiotensin II
  • Chronic kidney disease
  • Epithelial to mesenchymal transition
  • Renal fibrosis
  • Renin-angiotensin system

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