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.