Omentin-1 ameliorates pulmonary arterial hypertension by inhibiting endoplasmic reticulum stress through AMPKα signaling.
Clin Exp Hypertens
; 46(1): 2332695, 2024 Dec 31.
Article
in En
| MEDLINE
| ID: mdl-38527024
ABSTRACT
BACKGROUND:
Endothelial dysfunction of the pulmonary artery contributes to hypoxia-induced pulmonary arterial hypertension (PAH). Omentin-1, as a novel adipocytokine, plays an important protective role against cardiovascular diseases. However, the effect and underlying mechanisms of omentin-1 against PAH remain unclear.METHODS:
PAH was induced in SD (Sprague & Dawley) rats via a low-oxygen chamber for 4 weeks. Hemodynamic evaluation was undertaken using a PowerLab data acquisition system, and histopathological analysis was stained with hematoxylin and eosin (H&E). Endothelial function of pulmonary artery was assessed using wire myography.RESULTS:
We found that omentin-1 significantly improved pulmonary endothelial function in rats exposed to hypoxia and attenuated PAH. Mechanistically, we found that omentin-1 increased phosphorylated 5'adenosine monophosphateactivated protein kinase (pAMPK) level and reduced endoplasmic reticulum (ER) stress and increased NO production in pulmonary artery from rats exposed to hypoxia. However, the effect of omentin-1 was abolished by treatment with AMPK inhibitor (Compound C).CONCLUSIONS:
Our results reveal a protective effect of omentin-1 in PAH via inhibiting ER stress through AMPKα signaling and provide an agent with translational potential for the treatment of PAH.Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
AMP-Activated Protein Kinases
/
Pulmonary Arterial Hypertension
Limits:
Animals
Language:
En
Journal:
Clin Exp Hypertens
Year:
2024
Type:
Article
Affiliation country:
China