Angiotensin AT receptors reduce inflammation and fibrosis in cardiovascular remodeling.

The angiotensin AT2 receptor (ATR), an important member of the "protective arm" of the renin-angiotensin system (RAS), has been recently defined as a therapeutic target in different pathological conditions. The ATR activates complex signalling pathways linked to cellular proliferation, differentiation, anti-inflammation, antifibrosis, and induction or inhibition of apoptosis. The anti-inflammatory effect of ATR activation is commonly associated with reduced fibrosis in different models. Current discoveries demonstrated a direct impact of ATRs on the regulation of cytokines, transforming growth factor beta1 (TGF-beta1), matrix metalloproteases (MMPs), and synthesis of the extracellular matrix components. This review article summarizes current knowledge on the ATR in regard to immunity, inflammation and fibrosis in the heart and blood vessels. In particular, the differential influence of the ATR on cardiovascular remodeling in preclinical models of myocardial infarction, heart failure and aneurysm formation are discussed. Overall, these studies demonstrate that ATR stimulation represents a promising therapeutic approach to counteract myocardial and aortic damage in cardiovascular diseases.