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Related to atherogenesis: dyslipidemia


Formation of atheromatous deposits, especially on the innermost layer of arterial walls.

ath′er·o·gen′ic (-jĕn′ĭk) adj.
ath′er·o·gen·i′ci·ty (-jə-nĭs′ĭ-tē) n.
American Heritage® Dictionary of the English Language, Fifth Edition. Copyright © 2016 by Houghton Mifflin Harcourt Publishing Company. Published by Houghton Mifflin Harcourt Publishing Company. All rights reserved.
ThesaurusAntonymsRelated WordsSynonymsLegend:
Noun1.atherogenesis - the formation of atheromas on the walls of the arteries as in atherosclerosisatherogenesis - the formation of atheromas on the walls of the arteries as in atherosclerosis
pathology - any deviation from a healthy or normal condition
Based on WordNet 3.0, Farlex clipart collection. © 2003-2012 Princeton University, Farlex Inc.
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* They can help keep your arteries healthy, jury is still out on limes' effect on the arteries of humans, but a recent study found that lime juice and peel increased the plasma antioxidant capacity in rabbits, thus preventing or slowing down atherogenesis. The study also concluded that lime peel was more effective than lime juice.
[sPLA.sub.2]-11A production of fatty acids and biologically active phospholipids plays an important role in platelet, monocyte, and endothelial activation, processes known to be critical steps in atherogenesis. (6) Unlike traditional cardiac biomarkers used to predict adverse outcomes in patients with acute coronary syndrome (ACS), [sPLA.sub.2]-11A has been shown to act at multiple pathways involved in atherogenesis, from lipid oxidation to modulation of vascular and inflammatory cell activation and apoptosis.
Now, research from the University of Colorado Boulder has pinpointed a potential biological mechanism explaining the reverse of the medal - how lack of sleep affects circulation by promoting the build-up of fatty deposits in the arteries (atherogenesis), which can increase a person's risk of experiencing a stroke or heart attack.
1 Tissue factor (TF) is a protein that triggers the coagulation cascade, facilitating thrombosis and atherosclerosis.2,3 TF has been detected in various cell types within atheromatous plaques, including endothelial cells, vascular smooth muscle cells, monocyte, and, especially, macrophages, which account for about 60% of the total cells in the atheromatous plaque.1 TF found in the atheromatous lipid-core is thought to be largely derived from the macrophages present in the plaque.4 Macrophages contribute to thrombogenesis and atherogenesis partially via the mediation of TF.5 Under physiological conditions, macrophages express a low basal TF level.
However, after those high levels fall, patients taking diclofenac spend a substantial period of time with unopposed COX-2 inhibition, a state that is known to be prothrombotic, and also associated with blood pressure elevation, atherogenesis, and worsening of heart failure.
Increased levels of TC, TG with no change in HDL levels would be a compounding factor for increasing the risk of atherogenesis. [15] Thus, intervention in this age group would be of particular significance to prevent obesity-associated comorbidities and mortalities.
Psoriasis is associated with an accelerated risk of myocardial infarction and has increased risk for atherogenesis, which is the development of plaque within the walls of blood vessels.
Diabetes, lipid profile disorders, hypertension, and smoking are the common risk factors of atherogenesis, which result in the coronary artery disease [1].
Atherogenesis may lead to endothelial injury, owing to the oxidative stress and inflammation induced by the exposure to metabolic alterations and environmental factors including tobacco smoking, type 2 diabetes, hypertension, dyslipidemia, and obesity [5].
Moreover, HCV accelerates atherogenesis and is also associated with cardiovascular disorders [6].
HCAEC have previously been shown to exhibit increased responsiveness to inflammation and coagulation compared to HUVEC or human microvascular endothelial cells (HMVEC), which could account for greater susceptibility of coronary arteries to inflammation and atherogenesis leading to CV pathology [18].
Growing evidence supports a major role for nontraditional CVRFs in the pathogenesis of accelerated atherogenesis in this population (7).