AT2 receptor stimulation represents a promising therapeutic approach to counteract myocardial and aortic damage by reducing inflammation and fibrosis in cardiovascular diseases.
Does angiotensin AT2 receptor stimulation reduce inflammation and fibrosis in cardiovascular remodeling?
This review highlights the potential of AT2R stimulation as a therapeutic approach to reduce inflammation and fibrosis in cardiovascular diseases.
The angiotensin AT2 receptor (AT 2 R), 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 AT 2 R activates complex signalling pathways linked to cellular proliferation, differentiation, anti-inflammation, antifibrosis, and induction or inhibition of apoptosis. The anti-inflammatory effect of AT 2 R activation is commonly associated with reduced fibrosis in different models. Current discoveries demonstrated a direct impact of AT 2 Rs 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 AT 2 R in regard to immunity, inflammation and fibrosis in the heart and blood vessels. In particular, the differential influence of the AT 2 R on cardiovascular remodeling in preclinical models of myocardial infarction, heart failure and aneurysm formation are discussed. Overall, these studies demonstrate that AT 2 R stimulation represents a promising therapeutic approach to counteract myocardial and aortic damage in cardiovascular diseases.
Kaschina et al. (Sat,) conducted a review in Cardiovascular remodeling, myocardial infarction, heart failure, and aneurysm formation. AT2 receptor stimulation was evaluated. AT2 receptor stimulation represents a promising therapeutic approach to counteract myocardial and aortic damage by reducing inflammation and fibrosis in cardiovascular diseases.