Atherosclerosis is a pathological condition that underlies several important adverse vascular events such as stroke, cerebrovascular disease, Coronary Artery Disease (CAD). etc. [1]. It is responsible for most of the cardiovascular morbidity and mortality in the Western World currently [2]. As a result of the adoption of the western life style, its prevalence is increasing all over the world and could likely reach epidemic status in the coming future [2]. Atherosclerosis is a chronic disease of the arterial wall whose underlying pathogenesis involves an imbalanced lipid metabolism and a maladaptive immune response involving chronic inflammation of the arterial wall [1]. Leukocyte trafficking shapes the disturbed equilibrium of lipid accumulation, immune responses and their clearance and homeostasis, and this leukocyte trafficking is governed by chemokines and their receptors [1]. Chemokines are a superfamily of small structurally related chemotactic cytokines, which are involved in leukocyte trafficking and activation [3]. Chemokines have been found to play major roles in selectively recruiting monocytes, neutrophils, and lymphocytes, as well as in inducing chemotaxis through the activation of G-protein-coupled receptors [4]. Additionally, chemokines and their receptors have been identified as key players in the progression of atherosclerosis, thus they are explored in order to find therapeutic targets to prevent or treat Atherosclerosis and by targeting the chemokine system various entry points for a causative treatment are offered [5]. In this essay, the role of chemokine system in atherosclerosis is visited, the strategies employed to target chemokines as a therapeutic pathway for atherosclerosis and clinical trials undertaken ...
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12. Teupser D, Pavlides S, Tan M, Gutierrez-Ramos JC, Kolbeck R, & Breslow JL. (2004). Major reduction of atherosclerosis in fractalkine (CX3CL1)-deficient mice is at the brachiocephalic artery, not the aortic root. Proceedings of the National Academy of Sciences of the United States of America. 101, 17795-800.
13. Barlic J, & Murphy PM. (2007). Chemokine regulation of atherosclerosis. Journal of Leukocyte Biology. 82, 226-36.
14. Locati, M., Bonecchi, R., & Corsi, M. M. (2005). Chemokines and Their Receptors: Roles in Specific Clinical Conditions and Measurement in the Clinical Laboratory. PATHOLOGY PATTERNS REVIEWS. 123, S82-S95.
15. Bursill, C. A., Channon, K. M., & Greaves, D. R. (2004). The role of chemokines in atherosclerosis: recent evidence from experimental models and population genetics.Current Opinion in Lipidology. 15, 145-149.
The gaseous free radical nitric oxide is an abundant intracellular messenger molecule that plays a central role in maintenance of health, and is heavily involved in signal transduction in various cells of the body [1]. This molecule acts as a mediator in the regulation of cardiac function as well as having an important role in regulating contractility of the heart and maintenance of vascular tone in the cardiovascular system. As one of the most significant individuals in our discovery of nitric oxide, Dr. Robert Furchgott pioneered our understanding of this molecule through his experiments on the vasorelaxant properties of acetylcholine and the subsequent proposal of the presence of the endothelium derived relaxing factor, which was later identified to be nitric oxide [7]. Given the observation that cardiovascular disorders are the number one cause of death in many nations around the world, research into the vasorelaxant properties seems particularly relevant in order to help combat rising rates of vascular hypertension and high blood pressure. In this paper, the properties of nitric oxide are discussed largely with respect to the cardiovascular system. This paper focuses on the synthesis and characteristics of nitric oxide, the mechanisms of action by which nitric oxide works and the regulation of nitric oxide in the body, and finally a short summary of Robert Furchgott’s contributions to the discovery of nitric oxide and its properties.
Faries, D. E., Houston, J. P., Sulcs, E. N., & Swindle, R. W. (2012). A cross-validation of the provisional diagnostic instrument (PDI-4). BioMed Central, 13(1), 104. doi:10.1186/1471-2296-13-104
Kellermann, A., & Peleg, K. (2013, May 29). The New England journal of medicine. Retrieved from http://www.nejm.org/doi/full/10.1056/NEJMp1305304
“Immune Response: MedlinePlus Medical Encyclopedia.” National Library of Medicine - National Institutes of Health. Web. 18 Dec. 2011. .
Rang, H. P., Dale, M. M., Ritter, J. M., Flower, R. J., & Henderson, G. (2012). Pharmacology (7 ed.). London: Elsevier Inc.
Cardiovascular Diseases (CVD) are the currently the leading cause of death globally for both men and women accounting for 21.9 per cent of total deaths and is projected to increase to 26.3 per cent by 2030 . Statins are the treatment of choice for the primary and secondary prevention of cardiovascular disease and in the management of hypercholesterolaemia because of their proven efficacy and safety profile. Evidences are showing their effectiveness in reduction of cholesterol synthesis and number of pleiotropic effects, which may be cholesterol dependent and cholesterol independent. The present review focus on the origin, properties and effects of statins on endothelial function ( non lipid action of statins) through the increase of endogenous production of NO in different pathways.
2. Cytokines in Cancer Therapy. Francis R. Balkwill. Oxford University Press, NY, 1989. pp 1-8.
The hereditary risk factors for cardiovascular disease are primarily those of which individuals are unable to control, the ones for which they are born with. These risk factors would include an individual’s sex, race, age, and genetics. One out of every five males has some form of cardiovascular disease and the same applies for females. More women than men have cardiovascular disease in this country, but this is only due to the fact that there are more women within the U.S. population (Weiss and Lonnquist, 2011). Men percentage wise are at a higher risk than women. There is a somewhat reduced probability for females to have cardiovascular disease before menopause. This is believed by medical researchers and scientists to be directly related to the natural hor...
ICAM-1 is regularly used by the immune system to bind endothelial cells to leukocytes.
The risk of CVDs is usually predicated by a blood test that measures the level of lipoprotein because atherosclerosis is caused by high triglyceride levels, increases in low density lipoprotein (LDL) cholesterol levels, and decreases in high density lipoprotein (HDL) cholesterol levels (5). The majority of HDL consists of Apolipoprotein A-1 (ApoA-1) protein, where it exists mostly in the lipid-bound form in human plasma. ApoA-1 has anti-atherogenic properties (6), where it helps protect against the formation of abnormal fatty deposit within the walls of arteries. It has a specific role in lipid metabolism where it removes cholesterol from issues to the liver for excretion using a process called reverse cholesterol transport (7). Both ApoA-1
Atherosclerosis begins when the inner wall of the artery becomes damaged and cholesterol and fatty plaques begin to lodge in the arteries. Damage to the endothelial wall inside the artery can be caused by hypertension, hyperlipidemia, and hyperglycemia (“Subclinical Atherosclerosis..” 443). When this happens, the immune system responds by sending monocytes to the damaged area. The monocytes turn into macrophages; their job is to eat up the excess cholesterol and unblock the artery. The macrophages are unable to digest all of the cholesterol, and as a result turn in to foam cells. When many macrophages are turned into foam cells, plaque results, and protrudes into the arterial wall, restricting blood flow and raising blood pressure (“Atherosclerosis Growth Process.” 8). If the plaque becomes too large it may break, releasing plaque into the blood. This can cause a great reduction in blood flow or a clot, resulting in stroke or myocardial infarction (“Stroke Risk.” 3).
middle of paper ... ... Osman, Tagwa. Detection of Cytomorphological Changes in Oral Mucosa. NCBI. The.
The role of diet in Coronary artery disease is evident from its pathological process, which involves the formation of plaque within the arteries, alterations in endothelial (where the inner lining of the arteries don’t work properly) which in turn, influence blood pressure, and inflammatory processes. Diet plays a major role through the regulation of blood lipids and by influencing endothelial function and the underlying inflammation that causes disease progression. A modified diet, particularly if combined with regular exercise, can prevent, delay, or reverse the progression and development of CAD.
Cardiovascular disease (CVD) is a broad term covering a family of diseases linked by common risk factors and caused by atherosclerosis. These diseases include coronary heart disease, myocardial infarctions, heart failure, stroke, hypertension, hypercholesterolemia, diabetes, chronic kidney disease, peripheral artery disease, vascular dementia, and others included in ICD10 codes 100-199. CVD is the leading cause of death throughout the world, accounting for more than 17.5 million deaths in 2012; 31% of all global deaths [1]; more deaths than all forms of cancer combined. In 2013, CVD was the underlying cause of death for over 800,900 deaths, approximately 31% of all deaths in the United States [2]. In 2013 the overall attributable death
Atherosclerosis is the disease in which disease in which plaque builds up inside your arteries that are responsible in carrying oxygen-rich blood to heart and body. The plaques are formed by fat and cholesterol. To prevent atherosclerosis, the fat and cholesterol must be in low amount (Gibbon, 2013).