دورية أكاديمية
Lipoxygenase and prostaglandin G/H synthase cascades in cardiovascular disease.
| العنوان: | Lipoxygenase and prostaglandin G/H synthase cascades in cardiovascular disease. |
|---|---|
| المؤلفون: | Zhao L; Cordis Corp., a Johnson & Johnson company, 7 Powder Horn Drive, Warren, NJ 07059, USA. lzhao5@crdus.jnj.com, Grosser T, Fries S, Kadakia L, Wang H, Zhao J, Falotico R |
| المصدر: | Expert review of clinical immunology [Expert Rev Clin Immunol] 2006 Jul; Vol. 2 (4), pp. 649-58. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Taylor & Francis Country of Publication: England NLM ID: 101271248 Publication Model: Print Cited Medium: Internet ISSN: 1744-8409 (Electronic) Linking ISSN: 1744666X NLM ISO Abbreviation: Expert Rev Clin Immunol Subsets: PubMed not MEDLINE |
| أسماء مطبوعة: | Publication: 2015- : Abingdon, Oxford : Taylor & Francis Original Publication: London, UK : Future Drugs Ltd., 2005- |
| مستخلص: | The 12/15-lipoxygenase (LO) cascade governs the generation of 12-hydroperoxy-eicosatetraenoic acid (HPETE) and 15-HPETE from arachidonic acid. The 5-LO pathway plays a fundamental role in the biosynthesis of leukotrienes, essential inflammatory lipid mediators. Cyclooxygenase (COX)-1 and -2 biosynthetic pathways are responsible for prostaglandin and thromboxane formation. Experimental investigations in animal models using 12/15-LO deficient mice, 12/15-LO or 15-LO transgenic mice, or pharmacological 15-LO inhibition have all demonstrated the essential role of 12/15-LO in atherogenesis. The underlying mechanisms are linked to low-density lipoprotein oxidation, pro-inflammatory Th1 cytokine production and enhanced monocyte-endothelial cell interaction. Human genetic studies as well as disruption of the 5-LO gene in mouse models of hyperlipidemia revealed that 5-LO and 5-LO-activating protein are associated with risks of human cardiovascular disease, and that this cascade plays an important role in aortic aneurysm pathogenesis through leukotriene-mediated inflammatory chemokine production. COX-1 plays an active role in atherogenesis via thromboxane A(2), while COX-2-derived prostaglandin (PGI(2)) protects against atherosclerosis in murine models. Recent data demonstrated that selective inhibition of COX-2 augments the risk of cardiovascular events in patients. Selective inhibition or blockade of selective components in these two enzymatic pathways through systemic drug delivery or medical device approaches (e.g., drug-eluting stents) may have therapeutic benefit against certain cardiovascular diseases. |
| تواريخ الأحداث: | Date Created: 20100519 Date Completed: 20100609 Latest Revision: 20100518 |
| رمز التحديث: | 20240829 |
| DOI: | 10.1586/1744666X.2.4.649 |
| PMID: | 20477620 |
| قاعدة البيانات: | MEDLINE |
PDF full text from Publisher 
Full Text Finder | تدمد: | 1744-8409 |
|---|---|
| DOI: | 10.1586/1744666X.2.4.649 |