Essay on Role of Inflammation in Atherosclerosis

6. Atherosclerosis, pp.1157. is a form of arteriosclerosis in which thickening and hardening of the vessel are caused by the accumulation of lipid-laden macrophages w/I the arterial wall, which leads to the formation of a lesion called a plaque. It is not a single disease but rather a pathologic process that can affect vascular syustemns throughtout the body, resulting in ischemic syndromes that can vary widely in their severity and clinical manisfestations. It is the leading contributor to coronary artery and cerebrocascular disease. Athrosclerosis is an inflammatory disease, the lesions progress from endothelial injury and dysfunction

Atherosclerosis is associated with the major killer ailments in America, which include strokes, heart attacks, as well as peripheral vascular disease. The condition arises when there are a narrowing and hardening of the arteries. This is usually a gradual process, and it slowly blocks the arteries. When this happens, it will impede smooth blood flow. It is estimated that at least one million Americans lost their lives to a condition associated with atherosclerosis for the past few years.

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Cardiovascular disease (CVD) morbidity and mortality has reached epidemic proportions. Consequently, the importance of prevention of the disease, in addition to the treatment of the clinical outcome of the existing disease, has emerged as a priority in the field. These efforts have turned to what is in fact the underlying cause of myocardial infarctions and the resulting heart disease, specifically, atherosclerotic vascular disease.

Atherosclerosis disturbs the flow of blood and damages vessel endothelium causing an increase in platelet adherence. There is also an increased sensitivity by platelets to factors that cause adhesiveness and aggregation.

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The friable atheroma may rupture, or its surface may ulcerate, exposing its core to platelets and plasma coagulation factors which are activated and produce a thrombus or thromboembolus.

The development of an atherosclerotic plaque is relatively a very a complicated process where Plaque rupture accounts for about 76% of fatality lead by thrombi. The evolution of atherosclerosis begins with foam cell accumulation where the macrophages accumulate within arterial wall intima, progresses to form fatty streak where further accumulation of intra and extracellular lipids, this is a potentially reversible stage (Greenland p, 2013) further atheroma/fibroatheroma forms where cholesterol and phospholipids accumulate intramurally. This is a vulnerable state as it is predisposed to spontaneous rupture by inflammation and thrombus deposition may occur. Hemodynamic changes during this stage may cause ischemia or silent infarction, if large plaque rupture total occlusion may cause myocardial infarction or sudden cardiac death. Finally a complex lesion can develop where fibro muscular tissue can be seen with repair efforts followed by repeated plaque formation, this may slowly increase in size and produce significant arterial narrowing.

Two experimental systems will be used to determine if Mad1 overexpression promotes atherosclerosis. Both sets of experiments are routinely performed in the laboratory of Dr. Lian-Wang Guo and will be performed in collaboration with him. First, a mechanical injury model will be used to determine if elevated levels of Mad1 promote intimal hyperplasia. To generate the mechanical injury, mice will be anesthetized and undergo bilateral endoluminal injury to the femoral artery by passing a 0.25 mm diameter angioplasty guidewire 3 times 56. 1 and 3 days post-injury, protein expression will be determined by immunoblot. HA and Mad1 antibodies will be used to measure expression and localization of endogenous and inducible Mad1. PCNA will be used as a marker of VSMC proliferation.

Eagleton (2012) explains the pathological process inflammation has in weakening the arterial wall through the release of cellular and cytokine messengers which initiate various actions

These cells are able to produce and secrete such mediator molecules, like cytokines, chemokines, growth-factors, enzymes, and disintegrins, which activate endothelial cells, proliferation of smooth muscle cells, lesion progression, and the weakening of a vulnerable plaque by matrix degradation of its fibrous cap. Many of these molecules involved can be measured systemically and has been shown that elevated concentrations in the circulation are associated with future cardiovascular

Atherosclerosis is a lipid storage disease where too much of lipid is deposited in endothelial of arteries causing narrowing to prevent blood to flow. It is triggered by daily diet of consuming highly saturated fat, hypertension and smoking. In healthy endothelial cells, leukocytes do not stick on to the endothelial cells. During early phases of inflammation in endothelial cells, the leukocytes attach to the arteries cell wall with the help of vascular cell adhesion-1 (VCAM-1) and penentrate into the endothelial layer. VCAM-1 binds monocytes and T lymphocytes, the types of leukocytes found in early atherosclerotic plaques. ( Libby P., 2006:456S) Atherosclerosis lesion is a foam cells whereby macrophages engulf lipid particles. The lesion secretes cytokines and growth factors to promote proliferation of smooth muscle. The increased of inflammatory markers like interleukin 6 (IL-6) and interleukin 1 (IL-1) accumulated in the endothelial cells accerlate the progess of

Atherosclerosis is the leading cause of coronary heart disease, the number one killer of Americans (). The inflammatory process is known to lead to a myriad of other cardiovascular complications including, coronary heart disease, stroke and myocardial infarctions. It is important

The cardiovascular system is the network of blood vessels with the major role in transportation of oxygen and nutrition to the tissues and the waste products from organs and tissues. The diseases of the cardiovascular system, either acquired or congenital, may result in ischemia or undersupply of major organs, which would be a threat to the overall health of an individual. Events caused by cardiovascular diseases are the leading cause of morbidity and mortality worldwide. Despite improvements in the treatment and the preventive strategies of cardiovascular diseases, the social and economic burdens due to these diseases continue to grow. Further efforts, therefore,

Atherosclerosis is the process in which substances known as plaques, which are made up of cholesterol and platelets, adhere to tears in the walls of arteries. Over time these plaques build up to the point where they occlude blood flow in the arteries. When this happens in the coronary arteries, either directly, as the result of buildup in the arteries themselves, indirectly in the form a clot from another part of the body breaking loose and becoming lodged in the coronary arteries, the usual result is a heart attack.3