Conclusion
The present rat model of PAH showed elevated ACE protein levels in the lung as well as histopathological findings such as Increased intimal and medial fractions accompanied by obliterative lesions. DIZE, an ACE2 activator, reduced RVSP, medial wall thickness, and intimal fraction in pulmonary arterioles. In addition, it upregulates pulmonary expression of the ACE2/Ang-(1–7)/Mas receptor axis, leading to a therapeutic effect in this rat model of PAH. Our study showed that DIZE may be a potential agent for the treatment of PAH.