Authors
Mingyu Pu
Published in
Experimental lung research. Volume 52. Issue 1. Pages 182-195. Epub Sep 09, 2026.
Abstract
The fatality rate of pulmonary arterial hypertension (PAH) is high. This study aimed to determine the correlation between ACE2 and monocrotaline (MCT)-induced PAH in rats.
Rats were randomly divided into 4 groups: control group; MCT group; resorcinolnaphthalein (Rec) group; and Rec + A779 (Mas receptor antagonist) group. Rats in the control group received a single subcutaneous injection of normal saline on the 1st d, and an osmotic pump capsule combining normal saline subcutaneously since the 2nd d. The rats in the other 3 groups received a single subcutaneous injection of MCT on the 1st d. An osmotic minipumps containing normal saline, Rec, and Rec + A779 were implanted in rats in the MCT, Rec, and Rec + A779 groups, respectively.
The PAH rat model was successfully constructed with MCT. ACE2 reduced the mPAP, right ventricular hypertrophy index, and pulmonary artery media in the PAH rats (p < 0.05). Rec activated ACE2 expression and significantly increased the Mas levels, phospho-Akt (P-Akt), and phospho-eNOS (P-eNOS) in lung tissues of PAH rats (p < 0.05). The mPAP, right ventricular hypertrophy index, and pulmonary artery media in the Rec + A779 group were significantly increased compared to the blank and Rec groups (p < 0.05). The Mas level, P-Akt, and P-eNOS in rat lung tissues were significantly decreased in the Rec + A779 group compared to the Rec group (p < 0.05).
Rec upregulates ACE2 expression, and this elevated ACE2 expression may be associated with amelioration of MCT‑induced PAH in rats, likely through the downstream Akt/eNOS signaling pathway.
PMID:
42714327
Bibliographic data and abstract were imported from PubMed on 09 Sep 2026.
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