Anti-Inflammatory Effects of Epoxyeicosatrienoic Acids
Epoxyeicosatrienoic acids (EETs) are generated by the activity of both selective and also more general cytochrome p450 (CYP) enzymes on arachidonic acid and inactivated largely by soluble epoxide hydrolase (sEH), which converts them to their corresponding dihydroxyeicosatrienoic acids (DHETs). EETs...
Saved in:
| Main Authors: | , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2012-01-01
|
| Series: | International Journal of Vascular Medicine |
| Online Access: | http://dx.doi.org/10.1155/2012/605101 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832568185977569280 |
|---|---|
| author | Scott J. Thomson Ara Askari David Bishop-Bailey |
| author_facet | Scott J. Thomson Ara Askari David Bishop-Bailey |
| author_sort | Scott J. Thomson |
| collection | DOAJ |
| description | Epoxyeicosatrienoic acids (EETs) are generated by the activity of both selective and also more general cytochrome p450 (CYP) enzymes on arachidonic acid and inactivated largely by soluble epoxide hydrolase (sEH), which converts them to their corresponding dihydroxyeicosatrienoic acids (DHETs). EETs have been shown to have a diverse range of effects on the vasculature including relaxation of vascular tone, cellular proliferation, and angiogenesis as well as the migration of smooth muscle cells. This paper will highlight the growing evidence that EETs also mediate a number of anti-inflammatory effects in the cardiovascular system. In particular, numerous studies have demonstrated that potentiation of EET activity using different methods can inhibit inflammatory gene expression and signalling pathways in endothelial cells and monocytes and in models of cardiovascular diseases. The mechanisms by which EETs mediate their effects are largely unknown but may include direct binding to peroxisome proliferator-activated receptors (PPARs), G-protein coupled receptors (GPCRs), or transient receptor potential (TRP) channels, which initiate anti-inflammatory signalling cascades. |
| format | Article |
| id | doaj-art-f226f1247c24409ca99147af8f3e218b |
| institution | Kabale University |
| issn | 2090-2824 2090-2832 |
| language | English |
| publishDate | 2012-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Vascular Medicine |
| spelling | doaj-art-f226f1247c24409ca99147af8f3e218b2025-02-03T00:59:39ZengWileyInternational Journal of Vascular Medicine2090-28242090-28322012-01-01201210.1155/2012/605101605101Anti-Inflammatory Effects of Epoxyeicosatrienoic AcidsScott J. Thomson0Ara Askari1David Bishop-Bailey2Translational Medicine and Therapeutics, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UKTranslational Medicine and Therapeutics, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UKTranslational Medicine and Therapeutics, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UKEpoxyeicosatrienoic acids (EETs) are generated by the activity of both selective and also more general cytochrome p450 (CYP) enzymes on arachidonic acid and inactivated largely by soluble epoxide hydrolase (sEH), which converts them to their corresponding dihydroxyeicosatrienoic acids (DHETs). EETs have been shown to have a diverse range of effects on the vasculature including relaxation of vascular tone, cellular proliferation, and angiogenesis as well as the migration of smooth muscle cells. This paper will highlight the growing evidence that EETs also mediate a number of anti-inflammatory effects in the cardiovascular system. In particular, numerous studies have demonstrated that potentiation of EET activity using different methods can inhibit inflammatory gene expression and signalling pathways in endothelial cells and monocytes and in models of cardiovascular diseases. The mechanisms by which EETs mediate their effects are largely unknown but may include direct binding to peroxisome proliferator-activated receptors (PPARs), G-protein coupled receptors (GPCRs), or transient receptor potential (TRP) channels, which initiate anti-inflammatory signalling cascades.http://dx.doi.org/10.1155/2012/605101 |
| spellingShingle | Scott J. Thomson Ara Askari David Bishop-Bailey Anti-Inflammatory Effects of Epoxyeicosatrienoic Acids International Journal of Vascular Medicine |
| title | Anti-Inflammatory Effects of Epoxyeicosatrienoic Acids |
| title_full | Anti-Inflammatory Effects of Epoxyeicosatrienoic Acids |
| title_fullStr | Anti-Inflammatory Effects of Epoxyeicosatrienoic Acids |
| title_full_unstemmed | Anti-Inflammatory Effects of Epoxyeicosatrienoic Acids |
| title_short | Anti-Inflammatory Effects of Epoxyeicosatrienoic Acids |
| title_sort | anti inflammatory effects of epoxyeicosatrienoic acids |
| url | http://dx.doi.org/10.1155/2012/605101 |
| work_keys_str_mv | AT scottjthomson antiinflammatoryeffectsofepoxyeicosatrienoicacids AT araaskari antiinflammatoryeffectsofepoxyeicosatrienoicacids AT davidbishopbailey antiinflammatoryeffectsofepoxyeicosatrienoicacids |