Epoxyeicosatrienoic acids in cancer: a wake-up call

2012 ◽  
Author(s):  
Katrin Legg
Keyword(s):  
Epoxyeicosatrienoic Acids

1473-P: Circulating Epoxyeicosatrienoic Acids, Diabetes, and Cardiovascular Disease

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1473-P
Author(s):  
ROZENN N. LEMAITRE ◽  
PAUL N. JENSEN ◽  
MAXWELL B. ZEIGLER ◽  
AMANDA M. FRETTS ◽  
COLLEEN SITLANI ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Epoxyeicosatrienoic Acids

The interaction Between Arachidonic Acid Metabolism and Homocysteine

2020 ◽  
Vol 20 ◽  
Author(s):  
Elisa Domi ◽  
Malvina Hoxha ◽  
Bianka Hoxha ◽  
Bruno Zappacosta
Keyword(s):  
Cardiovascular Disease ◽  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Neurological Diseases ◽  
Arachidonic Acid Metabolism ◽  
Epoxyeicosatrienoic Acids ◽  
Pathological Conditions ◽  
Literature Searches ◽  
Hydroxyeicosatetraenoic Acids ◽  
Improve Health

Purpose: Hyperhomocysteinemia (HHcy) has been considered a risk factor for different diseases including cardiovascular disease (CVD), inflammation, neurological diseases, cancer and many other pathological conditions. Likewise, arachidonic acid (AA) metabolism is implicated in both vascular homeostasis and inflammation as shown by the development of CVD following the imbalance of its metabolites. Aim of The Review: This review summarizes how homocysteine (Hcy) can influence the metabolism of AA. Methods: In silico literature searches were performed on PubMed and Scopus as main sources. Results: Several studies have shown that altered levels of Hcy, through AA release and metabolism, can influence the synthesis and the activity of prostaglandins (PGs), prostacyclin (PGI₂), thromboxane (TXA), epoxyeicosatrienoic acids (EETs) and hydroxyeicosatetraenoic acids (HETEs). Conclusions: We believe that by targeting Hcy in AA pathways, novel compounds with better pharmacological and pharmacodynamics benefits may be obtained and that this information is valuable for dietician to manipulate diets to improve health.

scholarly journals Incorporation and distribution of epoxyeicosatrienoic acids into cellular phospholipids.

1992 ◽  
Vol 267 (6) ◽  
pp. 3686-3690 ◽  
Author(s):  
K Bernstrom ◽  
K Kayganich ◽  
R.C. Murphy ◽  
F.A. Fitzpatrick
Keyword(s):  
Epoxyeicosatrienoic Acids

Reno-protective mechanisms of epoxyeicosatrienoic acids in cardiovascular disease

2012 ◽  
Vol 302 (3) ◽  
pp. R321-R330 ◽  
Author(s):  
Ahmed A. Elmarakby
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Animal Models ◽  
Vascular Function ◽  
Organ Damage ◽  
Reduce Blood Pressure ◽  
Experimental Models ◽  
Epoxyeicosatrienoic Acids ◽  
Protective Effects ◽  
Protective Mechanisms

Cardiovascular disease (CVD) is the leading cause of mortality worldwide, and it is well known that end-stage renal disease (ESRD) is a profound consequence of the progression of CVD. Present treatments only slow CVD progression to ESRD, and it is imperative that new therapeutic strategies are developed to prevent the incidence of ESRD. Because epoxyeicosatrienoic acids (EETs) have been shown to elicit reno-protective effects in hypertensive animal models, the current review will focus on addressing the reno-protective mechanisms of EETs in CVD. The cytochrome P-450 epoxygenase catalyzes the oxidation of arachidonic acid to EETs. EETs have been identified as endothelium-derived hyperpolarizing factors (EDHFs) with vasodilatory, anti-inflammatory, antihypertensive, and antiplatelet aggregation properties. EETs also have profound effects on vascular migration and proliferation and promote angiogenesis. The progression of CVD has been linked to decreased EETs levels, leading to the concept that EETs should be therapeutically targeted to prevent end-organ damage associated with CVD. However, EETs are quickly degraded by the enzyme soluble epoxide hydrolase (sEH) to their less active diols, dihydroxyeicosatrienoic acids (DHETs). As such, one way to increase EETs level is to inhibit their degradation to DHETs by using sEH inhibitors. Inhibition of sEH has been shown to effectively reduce blood pressure and organ damage in experimental models of CVD. Another approach to target EETs is to develop EET analogs with improved solubility and resistance to auto-oxidation and metabolism by sEH. For example, stable ether EET analogs dilate afferent arterioles and lower blood pressure in hypertensive rodent animal models. EET agonists also improve insulin signaling and vascular function in animal models of metabolic syndrome.

scholarly journals Bradykinin-induced, endothelium-dependent responses in porcine coronary arteries: involvement of potassium channel activation and epoxyeicosatrienoic acids

2005 ◽  
Vol 145 (6) ◽  
pp. 775-784 ◽  
Author(s):  
Arthur H Weston ◽  
Michel Félétou ◽  
Paul M Vanhoutte ◽  
John R Falck ◽  
William B Campbell ◽  
...  
Keyword(s):  
Potassium Channel ◽  
Coronary Arteries ◽  
Epoxyeicosatrienoic Acids ◽  
Channel Activation

Effects of epoxyeicosatrienoic acids on polymorphonuclear leukocyte function

Life Sciences ◽  
2002 ◽  
Vol 70 (21) ◽  
pp. 2521-2533 ◽  
Author(s):  
Phillip F. Pratt ◽  
Mark Rosolowsky ◽  
William B. Campbell
Keyword(s):  
Polymorphonuclear Leukocyte ◽  
Epoxyeicosatrienoic Acids ◽  
Leukocyte Function
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