ArticleFrontiers in pharmacology2018
Deficiency of Soluble Epoxide Hydrolase Protects Cardiac Function Impaired by LPS-Induced Acute Inflammation.
Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 38 citations in OpenAlex.
- Article
- Adipokines as Cardioprotective Factors: BAT Steps Up to the Plate.Biomedicines · 2025Review
- The Octadecanoids: Synthesis and Bioactivity of 18-Carbon Oxygenated Fatty Acids in Mammals, Bacteria, and Fungi.Chemical reviews · 2025Review
- Intradomain Allosteric Regulation of Soluble Epoxide Hydrolase by Its Substrates.International journal of molecular sciences · 2024Article
- Oxylipins Derived from PUFAs in Cardiometabolic Diseases: Mechanism of Actions and Possible Nutritional Interactions.Nutrients · 2024Review
- The Cytochrome P450 2C8*3 Variant (rs11572080) Is Associated with Improved Asthma Symptom Control in Children and Altered Lipid Mediator Production and Inflammatory Response in Human Bronchial Epithelial Cells.Drug metabolism and disposition: the biological fate of chemicals · 2024Article
- The role of CYP-sEH derived lipid mediators in regulating mitochondrial biology and cellular senescence: implications for the aging heart.Frontiers in pharmacology · 2024Review
- Impact of Reperfusion on Plasma Oxylipins in ST-Segment Elevation Myocardial Infarction.Metabolites · 2023Article
- Article
- Cardiomyocyte-specific disruption of soluble epoxide hydrolase limits inflammation to preserve cardiac function.American journal of physiology. Heart and circulatory physiology · 2022Article
- Potential Cardioprotective Effects and Lipid Mediator Differences in Long-Chain Omega-3 Polyunsaturated Fatty Acid Supplemented Mice Given Chemotherapy.Metabolites · 2022Article
- Improved ELISA for linoleate-derived diols in human plasma utilizing a polyHRP-based secondary tracer.Analytical methods : advancing methods and applications · 2022Article
- Changes in the Left Ventricular Eicosanoid Profile in Human Dilated Cardiomyopathy.Frontiers in cardiovascular medicine · 2022Article
- A Novel Role for Cytochrome P450 Epoxygenase Metabolites in Septic Shock.Critical care explorations · 2022Article
- Effects of extracellular histones on left ventricular diastolic function and potential mechanisms in mice with sepsis.American journal of translational research · 2022Article
- Amelioration of Endotoxemia by a Synthetic Analog of Omega-3 Epoxyeicosanoids.Frontiers in immunology · 2022Article
- Managing SARS-CoV2 Infections Through Resolution of Inflammation by Eicosanoids: A Review.Journal of inflammation research · 2022Review
- Can N-3 polyunsaturated fatty acids be considered a potential adjuvant therapy for COVID-19-associated cardiovascular complications?Pharmacology & therapeutics · 2021Review
- Mitochondrial Lipid Signaling and Adaptive Thermogenesis.Metabolites · 2021Review
- Soluble Epoxide Hydrolase in Aged Female Mice and Human Explanted Hearts Following Ischemic Injury.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Lipopolysaccharide (LPS) is a bacterial wall endotoxin producing many pathophysiological conditions including myocardial inflammation leading to cardiotoxicity. Linoleic acid (18:2n6, LA) is an essential n-6 PUFA which is converted to arachidonic acid (20:4n6, AA) by desaturation and elongation via enzyme systems within the body. Biological transformation of PUFA through CYP-mediated hydroxylation, epoxidation, and allylic oxidation produces lipid mediators, which may be subsequently hydrolyzed to corresponding diol metabolites by soluble epoxide hydrolase (sEH). In the current study, we investigate whether inhibition of sEH, which alters the PUFA metabolite profile, can influence LPS induced cardiotoxicity and mitochondrial function. Our data demonstrate that deletion of soluble epoxide hydrolase provides protective effects against LPS-induced cardiotoxicity by maintaining mitochondrial function. There was a marked alteration in the cardiac metabolite profile with notable increases in sEH-derived vicinal diols, 9,10- and 12,13-dihydroxyoctadecenoic acid (DiHOME) in WT hearts following LPS administration, which was absent in sEH null mice. We found that DiHOMEs triggered pronounced mitochondrial structural abnormalities, which also contributed to the development of extensive mitochondrial dysfunction in cardiac cells. Accumulation of DiHOMEs may represent an intermediate mechanism through which LPS-induced acute inflammation triggers deleterious alterations in the myocardium
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