Either your web browser doesn't support Javascript or it is currently turned off. In the latter case, please turn on Javascript support in your web browser and reload this page. Classic atherosclerosis risk factors atherosclerosis khan academy not explain all cases of chronic heart disease. There is significant evidence that gut microbiota may influence the development https://digitales.com.au/blog/wp-content/custom/a-simple-barcoding-system-has-changed-inventory/who-coined-the-phrase-manifest-destiny-1.php atherosclerosis. The widespread prevalence of chronic Helicobacter pylori H.
Elevated production of reactive oxygen species during HP infection leads to cholesterol oxidation, which drives atherogenesis.
Introduction
The aim of this study is to explore the link between persistent HP infection and a high-fat diet in the atherosclerosis khan academy of proinflammatory conditions that are potentially proatherogenic. An in vivo model of Caviae porcellus infected with HP and exposed to an experimental diet was investigated for the occurrence of a proinflammatory and proatherogenic endothelial environment. Vascular endothelial primary cells exposed to HP atheroscleroosis were tested in vitro for oxidative stress, cell activation and apoptosis. The infiltration of inflammatory cells into the vascular endothelium of animals infected with HP and exposed to a high-fat diet was observed in conjunction with an increased level of inflammatory markers systemically.
Atheroscllerosis arteries of such animals were the least elastic, suggesting the role of HP in arterial stiffness. Soluble HP components induced transformation of macrophages to foam cells in vitro and influenced the endothelial life span, which was correlated with Collagen I upregulation. Atherosclerosis khan academy preliminary results support the hypothesis that HP antigens act synergistically with a high-fat diet in the development of proatherogenic conditions. Coronary heart disease CHD is one of the most severe chronic diseases of the coronary vessels, and an important health and social problem that is often life-threatening.
Materials and Methods
Classic risk factors of CHD include cigarette smoking, hypertension, diabetes mellitus and elevated levels of triglycerides and total cholesterol, especially the fraction of low-density lipoprotein LDL [ 12 ]. CHD develops due to endothelial dysfunction within the vessels, especially in the presence of elevated cholesterol and inflammation [ atherosclerosis khan academy ], which results in increased blood pressure, vascular wall remodeling, vascular inflammation development, increased platelet adhesion and aggregation. Such disorders promote the formation of atheromatous plaques, which are often unstable and subsequently rupture [ 2 ].
This might impair the blood flow leading to vascular blockage atherosclerosis khan academy myocardial infarction [ 1 ]. Importantly, classic risk factors for development of atherosclerosis do not explain taherosclerosis cases of CHD; therefore, the concept that atherogenesis may have an infectious background is extremely possible.
Chronic infections may influence the course of CHD via different mechanisms, such as chronic inflammatory reactions, autoimmune processes, and modification of the classic risk factors of CHD [ 45 ].]
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