Why the study?
Do EET agonists and sEH inhibitors improve endothelial and cardiac function in obesity-derived cardiovascular diseases?
Do EET agonists and sEH inhibitors improve endothelial and cardiac function in obesity-derived cardiovascular diseases?
Targeting the EET-HO pathway via EET agonists or sEH inhibitors represents a promising pharmacological strategy for mitigating obesity-related cardiovascular diseases.
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sEH inhibition to elevate EET may hold therapeutic potential in obesity-related CVD; leaves open the need for clinical trials.
The increase in the prevalence of obesity represents a worldwide phenomenon and is correlated with several metabolic and cardiovascular diseases, and cardiovascular disease remains the leading cause of death worldwide. And epoxyeicosatrienoic acid (EET), correlated with heme oxygenase (HO), with emerge to be a promising strategy for pharmacological mediation. Moreover, inhibit soluble epoxide hydroxylase (sEH), the enzyme converts EET to less potent metabolite, could upregulate EET concentration, which could upregulate HO-1, working together to reduce inflammation and increase vasodilation, in order to improve endothelial and cardiac function. The EET-HO pathway has been indicated as a most potent target for reversing oxidative stress and pre-adipocyte differentiation, so as to moderate oxidative capacity in mitochondrial dysfunction. While EET agonists and sEH inhibitors are becoming one of the potential therapies, and some of them are already in clinical trials. This review serves to summarize the ability of EET and HO pathway in attenuating the clinical impairments of obesity and associated cardiovascular diseases.
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Liu et al. (2018) studied this question.
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