Omentin-1 ameliorates pulmonary arterial hypertension by inhibiting endoplasmic reticulum stress through AMPKα signaling

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...

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Main Authors: Xinyu Deng, Hao Luo, Jing He, Wang Deng, Daoxin Wang
Format: Article
Language:English
Published: Taylor & Francis Group 2024-12-01
Series:Clinical and Experimental Hypertension
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Online Access:https://www.tandfonline.com/doi/10.1080/10641963.2024.2332695
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author Xinyu Deng
Hao Luo
Jing He
Wang Deng
Daoxin Wang
author_facet Xinyu Deng
Hao Luo
Jing He
Wang Deng
Daoxin Wang
author_sort Xinyu Deng
collection DOAJ
description 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 monophosphate‑activated protein kinase (p‑AMPK) 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.
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spelling doaj-art-e024bad2c59a4e1eb7c4ec01c22e03572025-08-20T02:35:50ZengTaylor & Francis GroupClinical and Experimental Hypertension1064-19631525-60062024-12-0146110.1080/10641963.2024.2332695Omentin-1 ameliorates pulmonary arterial hypertension by inhibiting endoplasmic reticulum stress through AMPKα signalingXinyu Deng0Hao Luo1Jing He2Wang Deng3Daoxin Wang4Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaDepartment of Cardiology, Daping Hospital, Third Military Medical University (Army Medical University), Chongqing, ChinaDepartment of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaDepartment of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaDepartment of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaBackground 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 monophosphate‑activated protein kinase (p‑AMPK) 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.https://www.tandfonline.com/doi/10.1080/10641963.2024.2332695Omentin-1pulmonary arterial hypertensionendoplasmic reticulum stressAMPKendothelial function
spellingShingle Xinyu Deng
Hao Luo
Jing He
Wang Deng
Daoxin Wang
Omentin-1 ameliorates pulmonary arterial hypertension by inhibiting endoplasmic reticulum stress through AMPKα signaling
Clinical and Experimental Hypertension
Omentin-1
pulmonary arterial hypertension
endoplasmic reticulum stress
AMPK
endothelial function
title Omentin-1 ameliorates pulmonary arterial hypertension by inhibiting endoplasmic reticulum stress through AMPKα signaling
title_full Omentin-1 ameliorates pulmonary arterial hypertension by inhibiting endoplasmic reticulum stress through AMPKα signaling
title_fullStr Omentin-1 ameliorates pulmonary arterial hypertension by inhibiting endoplasmic reticulum stress through AMPKα signaling
title_full_unstemmed Omentin-1 ameliorates pulmonary arterial hypertension by inhibiting endoplasmic reticulum stress through AMPKα signaling
title_short Omentin-1 ameliorates pulmonary arterial hypertension by inhibiting endoplasmic reticulum stress through AMPKα signaling
title_sort omentin 1 ameliorates pulmonary arterial hypertension by inhibiting endoplasmic reticulum stress through ampkα signaling
topic Omentin-1
pulmonary arterial hypertension
endoplasmic reticulum stress
AMPK
endothelial function
url https://www.tandfonline.com/doi/10.1080/10641963.2024.2332695
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