skip to main content
Language:
Search Limited to: Search Limited to: Resource type Show Results with: Show Results with: Search type Index

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

Clinical and experimental hypertension (1993), 2024-12, Vol.46 (1), p.2332695-2332695 [Peer Reviewed Journal]

ISSN: 1064-1963 ;EISSN: 1525-6006 ;DOI: 10.1080/10641963.2024.2332695 ;PMID: 38527024

Full text available

Citations Cited by
  • Title:
    Omentin-1 ameliorates pulmonary arterial hypertension by inhibiting endoplasmic reticulum stress through AMPKα signaling
  • Author: Deng, Xinyu ; Luo, Hao ; He, Jing ; Deng, Wang ; Wang, Daoxin
  • Subjects: AMP-Activated Protein Kinases - metabolism ; AMPK ; Animals ; Endoplasmic Reticulum Stress ; endothelial function ; Hypoxia - complications ; Hypoxia - metabolism ; Omentin-1 ; pulmonary arterial hypertension ; Pulmonary Arterial Hypertension - metabolism ; Pulmonary Artery ; Rats ; Rats, Sprague-Dawley ; Signal Transduction
  • Is Part Of: Clinical and experimental hypertension (1993), 2024-12, Vol.46 (1), p.2332695-2332695
  • Description: 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. 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. 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). 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.
  • Publisher: England: Taylor & Francis Group
  • Language: English
  • Identifier: ISSN: 1064-1963
    EISSN: 1525-6006
    DOI: 10.1080/10641963.2024.2332695
    PMID: 38527024
  • Source: MEDLINE
    DOAJ Directory of Open Access Journals
Back to results list
INSPIRE LIBRARY - TON DUC THANG UNIVERSITY (84-028) 37 755 057 Feedback
19 Nguyen Huu Tho St. Dist.7, HCM thuvien@tdtu.edu.vn

Copyright © 2017 INSPIRE LIBRARY - TON DUC THANG UNIVERSITY

Searching Remote Databases, Please Wait