Cardiomyocyte autophagy is regulated by angiotensin II type 1 and type 2 receptors

Porrello, Enzo R. and Delbridge, Lea M. D. (2009) Cardiomyocyte autophagy is regulated by angiotensin II type 1 and type 2 receptors. Autophagy, 5 8: 1215-1216. doi:10.4161/auto.5.8.10153

Author Porrello, Enzo R.
Delbridge, Lea M. D.
Title Cardiomyocyte autophagy is regulated by angiotensin II type 1 and type 2 receptors
Journal name Autophagy   Check publisher's open access policy
ISSN 1554-8627
Publication date 2009-11
Sub-type Editorial
DOI 10.4161/auto.5.8.10153
Volume 5
Issue 8
Start page 1215
End page 1216
Total pages 2
Place of publication Austin, TX, United States
Publisher Landes Bioscience
Language eng
Formatted abstract
Autophagic activity increases in the heart in response to a variety of stresses including hypertension, ischemia and neonatal starvation. Constitutive autophagy plays an important role in the maintenance of cellular homeostasis in the heart, whereas unrestrained autophagic activity accentuates the maladaptive cardiac remodeling response to stress (e.g. hypertension) and may contribute to the pathogenesis of heart failure. A detailed understanding of the molecular mechanisms governing autophagy induction and autophagosome maturation is evolving, but little is currently known about the extra- and intracellular cues that trigger autophagic induction in the heart. The renin-angiotensin system (RAS) is implicated in the pathogenesis of a number of cardiovascular conditions including hypertension, cardiac hypertrophy, myocardial infarction and heart failure. We now provide the first link between angiotensin II (AngII) and autophagy regulation in the heart. We demonstrate that AngII increases autophagosome formation via the AngII type I (AT1) receptor and that this response is constitutively antagonized by co-expression of the AngII type 2 (AT2) receptor in neonatal cardiomyocytes.
Keyword Angiotensin II
AT1 receptor
AT2 receptor
Cardiac hypertrophy
Q-Index Code CX
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Editorial
Collection: School of Biomedical Sciences Publications
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