ArticleFrontiers in pharmacology2014
PPARγ signaling is required for mediating EETs protective effects in neonatal cardiomyocytes exposed to LPS.
Article in Frontiers in pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- Soluble Epoxide Hydrolase Inhibition Confers Neuroprotection via PPAR-α Activation During Intracerebral Hemorrhage.Journal of neuroscience research · 2025Article
- Defined Diets Link Iron and α-Linolenic Acid to Cyp1b1 Regulation of Neonatal Liver Development Through Srebp Forms and LncRNA H19.International journal of molecular sciences · 2025Article
- Soluble epoxide hydrolase inhibition preserves alveolar bone in experimental periodontitis with estrogen deficiency.Frontiers in immunology · 2025Article
- Effects of sEH inhibition on the eicosanoid and cytokine storms in SARS-CoV-2-infected mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Regulation of soluble epoxide hydrolase in renal-associated diseases: insights from potential mechanisms to clinical researches.Frontiers in endocrinology · 2024Review
- CYP2C19 Contributes to THP-1-Cell-Derived M2 Macrophage Polarization by Producing 11,12- and 14,15-Epoxyeicosatrienoic Acid, Agonists of the PPARγ Receptor.Pharmaceuticals (Basel, Switzerland) · 2023Article
- 11,12-EET Regulates PPAR-γ Expression to Modulate TGF-β-Mediated Macrophage Polarization.Cells · 2023Article
- Cardiomyocyte-specific disruption of soluble epoxide hydrolase limits inflammation to preserve cardiac function.American journal of physiology. Heart and circulatory physiology · 2022Article
- COX-2/sEH Dual Inhibitor Alleviates Hepatocyte Senescence in NAFLD Mice by Restoring Autophagy through Sirt1/PI3K/AKT/mTOR.International journal of molecular sciences · 2022Article
- Clinical and Preclinical Evidence for Roles of Soluble Epoxide Hydrolase in Osteoarthritis Knee Pain.Arthritis & rheumatology (Hoboken, N.J.) · 2022Article
- TPPU treatment of burned mice dampens inflammation and generation of bioactive DHET which impairs neutrophil function.Scientific reports · 2021Article
- Article
- Development of multitarget agents possessing soluble epoxide hydrolase inhibitory activity.Prostaglandins & other lipid mediators · 2019Review
- Oxidized Lipids in Persistent Pain States.Frontiers in pharmacology · 2019Review
- Deficiency of Soluble Epoxide Hydrolase Protects Cardiac Function Impaired by LPS-Induced Acute Inflammation.Frontiers in pharmacology · 2018Article
- DHA and 19,20-EDP induce lysosomal-proteolytic-dependent cytotoxicity through de novo ceramide production in H9c2 cells with a glycolytic profile.Cell death discovery · 2018Article
- Attenuation of acute lung injury in a rat model by Semen Cassiae.BMC complementary and alternative medicine · 2017Article
- Inhibition of Soluble Epoxide Hydrolase Limits Mitochondrial Damage and Preserves Function Following Ischemic Injury.Frontiers in pharmacology · 2016Article
- Article
- CYP-epoxygenase metabolites of docosahexaenoic acid protect HL-1 cardiac cells against LPS-induced cytotoxicity Through SIRT1.Cell death discovery · 2015Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Lipopolysaccharide (LPS) is a bacterial wall endotoxin producing many pathophysiological conditions including myocardial inflammation leading to cardiotoxicity. Epoxyeicosatrienoic acids (EETs) are biologically active metabolites of arachidonic acids capable of activating protective cellular pathways in response to stress stimuli. EETs evoke a plethora of pathways limiting impairments of cellular structures, reducing cell death, and promoting anti-inflammatory reactions in various cell types. Considering EETs are capable of producing various biological protective effects, we hypothesized that EETs would protect rat neonatal cardiomyocytes (NCM) against LPS-induced cytotoxicity. In this study, we used a dual-acting, synthetic analog of EETs, UA-8 [13-(3-propylureido)tridec-8-enoic acid], possessing both EET-mimetic and soluble epoxide hydrolase selective inhibitory properties and 14,15-EET as a model of canonical EET molecules. We found that both UA-8 and 14,15-EET significantly improved cell viability and mitochondrial function of cardiomyocytes exposed to LPS. Furthermore, treatment with UA-8 or 14,15-EET resulted in significant attenuation of LPS-triggered pro-inflammatory response, caspase-3 activation and reduction in the total antioxidant capacity in cardiomyocytes. Importantly, EET-mediated effects were significantly reduced by pharmacological inhibition of peroxisome proliferator-activated receptors γ (PPARγ) suggesting that PPARγ signaling was required for EETs exerted protective effects. Data presented in the current study demonstrate that activation of PPARγ signaling plays a crucial role in EET-mediated protection against LPS-cytotoxicity in cardiomyocytes.
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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.