Key result
AT1 mediates angiotensin II-driven hypertrophy and fibrosis, whereas AT2 antagonizes these pathological actions.
Why the study?
The molecular mechanisms underlying activation and signal transduction of Ang II type 1 and type 2 receptors in the cardiovascular system require further elucidation.
Provides an overview of the opposing roles and molecular signaling mechanisms of AT1 and AT2 receptors in cardiovascular remodeling.
AT2 receptor effects may counter AT1-driven remodeling; leaves open targeted agonist development for clinical use.
The octapeptide angiotensin II (Ang II) plays a homeostatic role in the regulation of blood pressure and water and electrolyte balance, and also contributes to the progression of cardiovascular remodeling. Ang II activates Ang II type 1 (AT1) receptor and type 2 (AT2) receptor, both of which belong to the seven-transmembrane, G protein-coupled receptor family. Most of the actions of Ang II such as promotion of cellular prolifaration, hypertrophy, and fibrosis are mediated by AT1 receptor. However, in some pathological situations, AT2 receptor shows an increase in tissue expression and functions to antagonize the actions induced by AT1 receptor. Recent studies have advanced our understanding of the molecular mechanisms underlying receptor activation and signal transduction of AT1 and AT2 receptor in the cardiovascular system.
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Akazawa et al. (2013) conducted a review in Cardiovascular remodeling. Angiotensin II was evaluated. Angiotensin II mediates cellular proliferation, hypertrophy, and fibrosis primarily through the AT1 receptor, while the AT2 receptor antagonizes these actions in some pathological situations.
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