ArticlePulmonary circulation
Reciprocal actions of constrictor prostanoids and superoxide in chronic hypoxia-induced pulmonary hypertension: roles of EETs.
Article in Pulmonary circulation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Zinc, Soluble Epoxide Hydrolase, and the Pulmonary Vascular Paradox: Novel Insights into a Well-Known Phenomenon.American journal of respiratory and critical care medicine · 2025Article
- Zinc-mediated Inhibition of Soluble Epoxide Hydrolase Promotes Pulmonary Hypertension.American journal of respiratory and critical care medicine · 2025Article
- Omega-6 polyunsaturated fatty acids and their metabolites: a potential targeted therapy for pulmonary hypertension.Respiratory research · 2025Review
- Superoxide-Mediated Upregulation of MMP9 Participates in BMPR2 Destabilization and Pulmonary Hypertension Development.Antioxidants (Basel, Switzerland) · 2023Article
- Roles of Genetic Predisposition in the Sex Bias of Pulmonary Pathophysiology, as a Function of Estrogens : Sex Matters in the Prevalence of Lung Diseases.Advances in experimental medicine and biology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Epoxyeicosatrienoic acids (EETs) are synthesized from arachidonic acid by CYP/epoxygenase and metabolized by soluble epoxide hydrolase (sEH). Roles of EETs in hypoxia-induced pulmonary hypertension (HPH) remain elusive. The present study aimed to investigate the underlying mechanisms, by which EETs potentiate HPH. Experiments were conducted on sEH knockout (sEH-KO) and wild type (WT) mice after exposure to hypoxia (10% oxygen) for three weeks. In normal/normoxic conditions, WT and sEH-KO mice exhibited comparable pulmonary artery acceleration time (PAAT), ejection time (ET), PAAT/ET ratio, and velocity time integral (VTI), along with similar right ventricular systolic pressure (RVSP). Chronic hypoxia significantly reduced PAAT, ET, and VTI, coincided with an increase in RVSP; these impairments were more severe in sEH-KO than WT mice. Hypoxia elicited downregulation of sEH and upregulation of CYP2C9 accompanied with elevation of CYP-sourced superoxide, leading to enhanced pulmonary EETs in hypoxic mice with significantly higher levels in sEH-KO mice. Isometric tension of isolated pulmonary arteries was recorded. In addition to downregulation of eNOS-induced impairment of vasorelaxation to ACh, HPH mice displayed upregulation of thromboxane A
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.