Background
Pulmonary artery hypertension (PAH) is a life-threatening and
deteriorating disease with no promising therapy available currently due
to its diversity and complexity. An imbalance between vasoconstriction
and vasodilation has been proposed as the mechanism of PAH.
Angiotensin-converting enzyme 2 (ACE2), which catalyzes the hydrolysis
of the vasoconstrictor angiotensin (Ang) II into the vasodilator
Ang-(1-7), has been shown to be an important regulator of blood pressure
and cardiovascular diseases. Herein we hypothesized diminazene aceturate
(DIZE), an ACE2 activator, could ameliorate the development of PAH and
pulmonary vascular remodeling.