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(Hypertension. 2009;53:898.)
© 2009 American Heart Association, Inc.

Editorial Commentaries

Angiotensin Receptors and Autophagy

Live and Let Die

U. Muscha Steckelings; Thomas Unger

From the Center for Cardiovascular Research, Institute of Pharmacology, Charité-Universitätsmedizin Berlin, Berlin, Germany.

Correspondence to U. Muscha Steckelings, Center for Cardiovascular Research, Institute of Pharmacology, Charité-Universitätsmedizin Berlin, Hessische Str 3-4, 10115 Berlin, Germany. E-mail ulrike.steckelings@charite.de

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The renin-angiotensin system (RAS) and autophagy are both essentially involved in the pathomechanisms of various cardiovascular pathologies, eg, cardiac hypertrophy/load-induced heart disease, ischemic heart disease, or atherosclerosis.^1–4 Regarding the RAS, it is commonly accepted that angiotensin II via the angiotensin II type 1 receptor (AT₁R) directly and indirectly (by increasing blood pressure) contributes to, eg, cardiomyocyte hypertrophy, interstitial fibrosis, inflammation, oxidative stress, or apoptosis in cardiac pathologies, thereby promoting disease.^1,5 In contrast, regarding the angiotensin II type 2 receptor (AT₂R), the majority of data points to a tissue-protective effect of this receptor in cardiac disease because of its antifibrotic, anti-inflammatory, and antiapoptotic features. However, some publications also report a prohypertrophic effect of the AT₂R in the heart. Because the determination of "true" AT₂R-mediated effects is still difficult and experimental approaches are often indirect (inhibition experiments using the AT₂R antagonist PD123319) and/or make use of genetically altered animals or cells, the true nature of AT₂R-mediated effects in cardiac diseases is probably not yet completely understood.

Autophagy represents a highly conserved process for the lysosomal degradation of cytoplasmatic long-lived proteins and organelles.⁶ It can result in final decomposition of proteins contributing to a certain form of programmed cell death (autophagic cell death), but it may also serve as a survival mechanism by intracellular clearance of toxic or damaged proteins and organelles or, in times of starvation, through protein recycling and maintenance of intermediary metabolism.⁶ During autophagy, autophagosomes are built from so-called isolated membranes to sequestrate . . . [Full Text of this Article]

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Angiotensin II Type 2 Receptor Antagonizes Angiotensin II Type 1 Receptor–Mediated Cardiomyocyte Autophagy

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Hypertension 2009 53: 1032-1040. [Abstract] [Full Text] [PDF]