AT2 Receptors Targeting Cardiac Protection Post-Myocardial Infarction

Elena Kaschina, Dilyara Lauer, Patrick Schmerler, Thomas Unger, U. Muscha Steckelings*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


The angiotensin AT2-receptor mediates tissue protective actions. Its regenerative potential has been tested in multiple disease models including models of myocardial infarction. These studies used different experimental approaches in order to detect AT2-receptor-related effects such as AT2-receptor deficiency or overexpression, treatment with an AT1-receptor blocker leading to indirect stimulation of the unopposed AT2-receptor, or studies using AT2-receptor agonists. It is a common finding in these studies that the AT2-receptor improves cardiac function in the early phase post-MI, and that this effect is preserved over periods of up to four months. Depending on the experimental protocol, the AT2R also attenuates post-MI left ventricular remodeling or protects the heart from early left ventricular thinning and rupture. In combination with AT1-receptor blockade or deficiency, post-MI cardiac hypertrophy is reduced. This article reviews studies on the role of the AT2-receptor in myocardial infarction with an emphasis on the most recent data obtained in studies using AT2-receptor agonists.
Original languageEnglish
Article number441
JournalCurrent Hypertension Reports
Issue number7
Publication statusPublished - Jul 2014


  • Angiotensin
  • AT2-receptor
  • Myocardial infarction
  • Left ventricular remodeling
  • Cardiac hypertrophy


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