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https://olympias.lib.uoi.gr/jspui/handle/123456789/9736Full metadata record
| DC Field | Value | Language |
|---|---|---|
| dc.contributor.author | Tselepis, A. D. | en |
| dc.contributor.author | Rizzo, M. | en |
| dc.contributor.author | Goudevenos, I. A. | en |
| dc.date.accessioned | 2015-11-24T16:51:28Z | - |
| dc.date.available | 2015-11-24T16:51:28Z | - |
| dc.identifier.issn | 1381-6128 | - |
| dc.identifier.uri | https://olympias.lib.uoi.gr/jspui/handle/123456789/9736 | - |
| dc.rights | Default Licence | - |
| dc.subject | atherosclerosis | en |
| dc.subject | cardiovascular disease | en |
| dc.subject | darapladib | en |
| dc.subject | inflammation | en |
| dc.subject | lipoproteins | en |
| dc.subject | lp-pla2 | en |
| dc.subject | platelet-activating-factor | en |
| dc.subject | low-density-lipoprotein | en |
| dc.subject | coronary-artery-disease | en |
| dc.subject | factor-acetylhydrolase activity | en |
| dc.subject | atherosclerotic plaque | en |
| dc.subject | rheumatoid-arthritis | en |
| dc.subject | heart-disease | en |
| dc.subject | cardiovascular-disease | en |
| dc.subject | secondary prevention | en |
| dc.subject | risk-assessment | en |
| dc.title | Therapeutic Modulation of Lipoprotein-associated Phospholipase A2 (Lp-PLA2) | en |
| heal.type | journalArticle | - |
| heal.type.en | Journal article | en |
| heal.type.el | Άρθρο Περιοδικού | el |
| heal.identifier.secondary | <Go to ISI>://000299638000006 | - |
| heal.language | en | - |
| heal.access | campus | - |
| heal.recordProvider | Πανεπιστήμιο Ιωαννίνων. Σχολή Θετικών Επιστημών. Τμήμα Χημείας | el |
| heal.publicationDate | 2011 | - |
| heal.abstract | Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a calcium-independent phospholipase A2 that circulates in plasma in association with lipoprotein particles, whereas in atherosclerotic plaques it is co-localized with macrophages. Lp-PLA2 generates two proinflammatory mediators, lysophosphatidylcholine and oxidized nonesterified fatty acids, which play a role in the development of atherosclerotic lesions and formation of a necrotic core, leading to more vulnerable plaques. Epidemiologic studies demonstrate that increased circulating levels of Lp-PLA2 predict an increased risk of myocardial infarction, stroke and cardiovascular mortality. Furthermore, histologic examination of diseased human coronary arteries reveals intense presence of the enzyme in atherosclerotic plaques that are prone to rupture. These considerations suggest Lp-PLA2 as a promising therapeutic target in cardiovascular disease. Plasma levels of Lp-PLA2 are increased in various types of hyperlipidemias, while hypolipidemic drugs reduce plasma Lp-PLA2 activity and mass along with the improvement of plasma lipid profile. A selective inhibitor of Lp-PLA2 activity, darapladib, has been developed and studies in animal models and humans have shown that it effectively and safely reduces Lp-PLA2 activity in plasma and in atherosclerotic plaques. Furthermore, in animal models darapladib decreases plaque area and necrotic core area whereas in humans it prevents the expansion of necrotic core volume. Whether the results obtained from the use of darapladib in studies in vitro, as well as in preclinical and clinical studies would translate into benefits on cardiovascular event outcomes, awaits to be proved in 2 ongoing phase 3 trials. | en |
| heal.journalName | Curr Pharm Des | en |
| heal.journalType | peer reviewed | - |
| heal.fullTextAvailability | TRUE | - |
| Appears in Collections: | Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά). ΧΗΜ | |
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