ReviewAmerican journal of physiology. Heart and circulatory physiology2009
Role of arachidonic acid lipoxygenase metabolites in the regulation of vascular tone.
Review in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
58 citing papers in PubMed, 115 citations in OpenAlex.
- GPX4 alleviates airway inflammation by suppressing 5-LO expression and regulating ferroptosis.Respiratory research · 2026Article
- CYP2C19 intermediate and poor metabolizer statuses may be associated with coronary atherosclerosis among patients with type 2 diabetes mellitus.Frontiers in medicine · 2026Article
- Clinical and Genetic Factors Associated with Multivessel Coronary Artery Disease: A Cross-Sectional Study of CYP2C19 Polymorphisms and Metabolic Comorbidities.International journal of general medicine · 2026Article
- CYP2C19 Loss-of-Function Is an Independent Risk Factor of Coronary Artery Disease in Patients With Hypertension.Journal of clinical laboratory analysis · 2025Article
- 12/15-lipoxygenase mediates disturbed flow-induced endothelial dysfunction and atherosclerosis.Molecular medicine (Cambridge, Mass.) · 2025Article
- Roles of Lipoxygenases in Cardiovascular Diseases.Journal of cardiovascular translational research · 2025Review
- Omega-6 polyunsaturated fatty acids and their metabolites: a potential targeted therapy for pulmonary hypertension.Respiratory research · 2025Review
- Dynamics of oxylipin biosynthesis in systemic inflammation: insights from a large animal model of endotoxemia.Frontiers in immunology · 2025Article
- CYP2C19 loss-of-function variants are independent risk factors for premature cerebral infarction: a hospital based retrospective study.BMC cardiovascular disorders · 2024Article
- Mechanisms of Abnormal Lipid Metabolism in the Pathogenesis of Disease.International journal of molecular sciences · 2024Review
- Bazi Bushen ameliorates age-related energy metabolism dysregulation by targeting the IL-17/TNF inflammatory pathway associated with SASP.Chinese medicine · 2024Article
- Article
- CYP2C19 Poor Metabolizer Status and High System Inflammation Response Index are Independent Risk Factors for Premature Myocardial Infarction: A Hospital-Based Retrospective Study.International journal of general medicine · 2024Article
- ProbioticsmSystems · 2023Article
- Fetal metabolic adaptations to cardiovascular stress in twin-twin transfusion syndrome.iScience · 2023Article
- CYP2C19 loss-of-function is associated with increased risk of hypertension in a Hakka population: a case-control study.BMC cardiovascular disorders · 2023Article
- Classes of Lipid Mediators and Their Effects on Vascular Inflammation in Atherosclerosis.International journal of molecular sciences · 2023Review
- Differences in the Proportion of CYP2C19 Loss-of-Function Between Cerebral Infarction and Coronary Artery Disease Patients.International journal of general medicine · 2023Article
- Article
- Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Stimulation of vascular endothelial cells with agonists such as acetylcholine (ACh) or bradykinin or with shear stress activates phospholipases and releases arachidonic acid (AA). AA is metabolized by cyclooxygenases, cytochrome P-450s, and lipoxygenases (LOs) to vasoactive products. In some arteries, a substantial component of the vasodilator response is dependent on LO metabolites of AA. Nitric oxide (NO)- and prostaglandin (PG)-independent vasodilatory responses to ACh and AA are reduced by inhibitors of LO and by antisense oligonucleotides specifically against 15-LO-1. Vasoactive 15-LO metabolites derived from the vascular endothelium include 15-hydroxy-11,12-epoxyeicosatrienoic acid (15-H-11,12-HEETA) that is hydrolyzed by soluble epoxide hydrolase to 11,12,15-trihydroxyeicosatrienoic acid (11,12,15-THETA). HEETA and THETA are endothelium-derived hyperpolarizing factors that induce vascular relaxations by activation of smooth muscle apamin-sensitive, calcium-activated, small-conductance K(+) channels causing hyperpolarization. In other arteries, the 12-LO metabolite 12-hydroxyeicosatetraenoic acid is synthesized by the vascular endothelium and relaxes smooth muscle by large-conductance, calcium-activated K(+) channel activation. Thus formation of vasodilator eicosanoids derived from LO pathways contributes to the regulation of vascular tone, local blood flow, and blood pressure.
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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.