ArticleAmerican journal of physiology. Heart and circulatory physiology2015
Soluble epoxide hydrolase inhibition improves coronary endothelial function and prevents the development of cardiac alterations in obese insulin-resistant mice.
Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 53 citations in OpenAlex.
- PTUPB, a soluble epoxide hydrolase/cyclooxygenase‑2 dual inhibitor, reduces endothelial‑to‑mesenchymal transition and improves doxorubicin‑induced vascular and cardiac toxicity.Molecular medicine reports · 2026Article
- Liquid Chromatography-Tandem Mass Spectrometry-Based Targeted Lipidomic Analysis of Obesity-Related Colorectal Cancer: Potential Roles of the CYP Eicosanoid Pathway.The Journal of nutrition · 2026Article
- Alterations in Epoxyeicosatrienoic Acids Metabolism in Type 2 Diabetes Mellitus and Potential Association with Retinopathy Progression.Current medicinal chemistry · 2026Article
- Alpha-7 nicotinic acetylcholine receptor: targeting the interplay between inflammation, renin-angiotensin aldosterone system, and nervous system for the novel treatment of heart failure.Frontiers in pharmacology · 2026Review
- The mineralocorticoid receptor antagonist finerenone enhances cardiovascular recovery upon food intake normalization in obese mice.Cardiovascular diabetology · 2025Article
- Cardiometabolic Phenotype in HFpEF: Insights from Murine Models.Biomedicines · 2025Review
- Inhibition of cytochrome P450 epoxygenase promotes endothelium-to-mesenchymal transition and exacerbates doxorubicin-induced cardiovascular toxicity.Molecular biology reports · 2024Article
- Sex-Specific Response of the Brain Free Oxylipin Profile to Soluble Epoxide Hydrolase Inhibition.Nutrients · 2023Article
- CRISPR/Cas9-mediated inactivation of the phosphatase activity of soluble epoxide hydrolase prevents obesity and cardiac ischemic injury.Journal of advanced research · 2023Article
- High Glycemia and Soluble Epoxide Hydrolase in Females: Differential Multiomics in Murine Brain Microvasculature.International journal of molecular sciences · 2022Article
- CYP450 Epoxygenase Metabolites, Epoxyeicosatrienoic Acids, as Novel Anti-Inflammatory Mediators.Molecules (Basel, Switzerland) · 2022Review
- Heme-oxygenase and lipid mediators in obesity and associated cardiometabolic diseases: Therapeutic implications.Pharmacology & therapeutics · 2022Review
- Epoxylipids and soluble epoxide hydrolase in heart diseases.Biochemical pharmacology · 2022Review
- MRI-based in vivo detection of coronary microvascular dysfunction before alterations in cardiac function induced by short-term high-fat diet in mice.Scientific reports · 2021Article
- Vascular effects of disrupting endothelial mTORC1 signaling in obesity.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- Soluble epoxide hydrolase deficiency attenuates lipotoxic cardiomyopathy via upregulation of AMPK-mTORC mediated autophagy.Journal of molecular and cellular cardiology · 2021Article
- Preservation of epoxyeicosatrienoic acid bioavailability prevents renal allograft dysfunction and cardiovascular alterations in kidney transplant recipients.Scientific reports · 2021Article
- Wnt Signaling Cascades and Their Role in Coronary Artery Health and Disease.Journal of cellular signaling · 2021Article
- Soluble epoxide hydrolase as a therapeutic target for obesity-induced disorders: roles of gut barrier function involved.Prostaglandins, leukotrienes, and essential fatty acids · 2020Review
- Soluble Epoxide Hydrolase Inhibition byInternational journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
Abstract
This study addressed the hypothesis that inhibiting the soluble epoxide hydrolase (sEH)-mediated degradation of epoxy-fatty acids, notably epoxyeicosatrienoic acids, has an additional impact against cardiovascular damage in insulin resistance, beyond its previously demonstrated beneficial effect on glucose homeostasis. The cardiovascular and metabolic effects of the sEH inhibitor trans-4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid (t-AUCB; 10 mg/l in drinking water) were compared with those of the sulfonylurea glibenclamide (80 mg/l), both administered for 8 wk in FVB mice subjected to a high-fat diet (HFD; 60% fat) for 16 wk. Mice on control chow diet (10% fat) and nontreated HFD mice served as controls. Glibenclamide and t-AUCB similarly prevented the increased fasting glycemia in HFD mice, but only t-AUCB improved glucose tolerance and decreased gluconeogenesis, without modifying weight gain. Moreover, t-AUCB reduced adipose tissue inflammation, plasma free fatty acids, and LDL cholesterol and prevented hepatic steatosis. Furthermore, only the sEH inhibitor improved endothelium-dependent relaxations to acetylcholine, assessed by myography in isolated coronary arteries. This improvement was related to a restoration of epoxyeicosatrienoic acid and nitric oxide pathways, as shown by the increased inhibitory effects of the nitric oxide synthase and cytochrome P-450 epoxygenase inhibitors l-NA and MSPPOH on these relaxations. Moreover, t-AUCB decreased cardiac hypertrophy, fibrosis, and inflammation and improved diastolic function, as demonstrated by the increased E/A ratio (echocardiography) and decreased slope of the end-diastolic pressure-volume relation (invasive hemodynamics). These results demonstrate that sEH inhibition improves coronary endothelial function and prevents cardiac remodeling and diastolic dysfunction in obese insulin-resistant mice.
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