Essay On Atherosclerosis

Atherosclerosis is a disease in which fatty materials and plaque buildup on the inner lining of arteries. Arteries are blood vessels which carry rich blood to the heart and throughout the body. They’re lined by the endothelium, a thin layer of cells. The endothelium keeps blood flowing by keeping the inside of arteries smooth. However, when Atherosclerosis starts due to high blood pressure, smoking, or high cholesterol, it damages the endothelium. Atherosclerosis tends to happen throughout the body and arises when people grow older. This disease is mainly due to the deposition of fatty materials i.e., cholesterol, calcium and other substances found in the blood. The buildup of fat then hardens causing narrowing of the arteries. This

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 a chronic disease that can beginning in childhood or adolescence. Atherosclerosis is defined as a buildup of fatty material, such as cholesterol, in the walls of blood vessels. There are three progressive states of excess fatty material in the blood vessel walls: fatty streak, intermediate lesion, and a fibrous lesion. A fatty streak is a line of yellow fatty material in the blood vessel wall, and as the streak becomes larger it is then called an intermediate lesion then a fibrous lesion. A fibrous lesion can be occlusive of non-occlusive. The occlusive lesion forms under the endothelium of the blood vessel and grows towards the lumen of the blood vessel cause the lumen to become smaller. A non-occlusive lesion forms under

Immune processes are involved in the development and progression of atherosclerotic lesions. Healthy endothelial cells release nitric oxide to stimulate vasodilation, avoid microphage infiltration, and to slow the increase of vascular smooth muscle cells. These mechanisms help protect against

Although it was believed for a long time that second-hand smoke only affects smokers, since the early 1980s it has been known that non-smoking family members of smokers have twice the risk of experiencing heart attacks than those in non-smoking households. Consequently, people living and working in environments that contain second-hand smoke suffer coronary heart diseases (CHD) due to the toxic substances of tobacco smoke.

This is lead to heart attack, stroke and some kind of organ failure. One of most importance event cellular migration that contributes to plaque development in atherosclerosis. During cell migration Filamin A cross-links F-actin filamints in leading edgs of the migrating cells and also has been shown to regulate signal transduction. Macrophages are present in atherosclerotic plaque and have the migratory properties that complicate atherogenesis.

Arteries carry blood from the heart to the rest of the body. A thin layer of cells allows blood to flow easily and it’s called the endothelium. Atherosclerosis begins when the endothelium becomes damaged allowing bad cholesterol to build up in the artery wall. The body sends white blood cells to clean up the bad cholesterol but sometimes the cells get stuck at the affected site. Over time plaque can accumulate, made up of cholesterol, macrophages, calcium, and other substances from the blood. Can be fatal if not treated.

Integrin Signaling in Endothelial Cell Activation. In quiescent vessels, the endothelial layer regulates vascular tone, provides an anti-thrombotic surface, and forms a tight barrier to restrict the passage of blood components into surrounding tissue [39]. Activation of the endothelial cell layer during inflammatory responses involves a phenotypic transition that increases vascular permeability and enhances the expression of leukocyte counter-receptors (e.g. ICAM-1, VCAM-1), proinflammatory cytokines (tumor necrosis factor α (TNFα), interleukin-1B (IL-1β)), and pro-coagulant molecules (tissue factor (TF)) [39]. Molecularly, endothelial activation represents the first discernable sign of local atherosclerotic susceptibility and is maintained during subsequent stages of atherosclerotic progression [40]. Several stimuli promote endothelial activation, including mechanical stress, oxidized LDL (oxLDL), proinflammatory cytokines (e.g. TNFα, IL-1β), and the bacterial endotoxin LPS [39]. Much of the reprogramming in endothelial gene expression can be attributed to the proinflammatory transcription factor nuclear factor-κB (NF-κB) [41, 42]. The NF-B family of homodimeric and heterodimeric transcription factors is maintained in an inactive state in the cytoplasm but translocates to the nucleus upon activation in response to a variety of endothelial cell activators

As of late VEGF expression has been exhibited in heart myofibroblasts, non-endothelial cells with the morphological elements of fibroblasts. Myofibroblasts assume a noteworthy part in the development, improvement and repair of typical tissue and are found at the site of localized necrosis. RT-PCR, Northern blot and Western blot investigation affirmed the vicinity of mRNA and protein for VEGF, VEGFR-1 (VEGF receptor 1 otherwise called Flt-1, fms-like tyrosine kinase) and VEGFR-2 (KDR/Flk-1, fetal liver kinase 1 is the murine homologue of human Kinase embed Area containing Receptor) in rodent myofibroblasts segregated from heart infarcts.10 Coexpression of VEGF and its receptors on the myofibroblasts proposes that VEGF adds to tissue rebuilding at the site of dead tissue in an autocrine way. VEGF might likewise assume a part in atherosclerosis. Uptake of oxidized low-thickness lipoprotein (bull LDL) by macrophages starts froth cell development in atherosclerotic sores. Oxidized LDL expanded VEGF creation by the U937 monocyte cell line and by macrophages. As VEGF likewise increments vascular penetrability, VEGF creation by froth cells and macrophages may bother atherosclerosis by improving vessel porousness to

Atherosclerosis is the leading cause of death in the world. This pathology is an inflammatory disease that results from an initial

Figure 3. Roles of eNOS in atherosclerosis. The structure of NOS is a homodimer with each monomer including an oxygenase dominion and a reductase dominion. The oxygenase dominion comprises the binding locates for heme, L-arginine (the substrate) and the cofactor tetrahydrobiopterin (BH4), an important determining factor of eNOS activity. In vascular disease states such as diabetes, hypertension, or hypercholesterolemia, superoxide generation by oxidases is significantly increased. Peroxynitrite and other reactive oxygen species oxidize BH4, through the BH3 radical to BH2 and biopterin, which decreases the bioavailability of BH4 and stimulates eNOS uncoupling. This form of eNOS no longer produces NO, but instead produces superoxide.

It is known that inflammation plays an important role in the development of atherosclerosis. Inflammatory mediators have been found in areas of atheroma formation. Currently, a link between lipids and inflammation have been the most applicable explication for atherogenesis.

According to World Health Organization (WHO), Centers for Disease Control (CDC) and American Heart Association (AHA), Cardiovascular disease (CVD) is the major cause of mortality worldwide. The primary contributor to coronary artery disease and resulting cardiovascular complications pathogenesis of atherosclerosis, Atherosclerosis is chronic inflammatory process of deposition of fatty cholesterol filled plaque in arterial wall which narrows the diameter and obstructs blood flow down the length of coronary artery and throughout its branches. Nowadays, micronutrients are been studied extensively for minimizing risk intervention of CVD. Among these, dietary supplements antioxidants available over the counter are highly commercialized but scientific

Katarzyna, Sherine, Garry, Derek, Stephen James, and Ian (2015), authors of the article “Antioxidants in cardiovascular therapy: Panacea or false hope?”, re-examined the roles played by antioxidants such as vitamins A, C, and E, folic acid and other B vitamins, polyphenols, mineral such as selenium, drugs such as N-Acetylcysteine (NAC) and allopurinol in regards to their therapeutic properties to combat various illnesses such as heart diseases, ischemic strokes, and peripheral arterial disease. Katarzyna et al. (2015) also explored the setbacks related to the antioxidants’ properties in the cardiovascular disease prevention and management as well as the myths and merits linked to this research topic. The researchers compared the data gathered

Atherosclerosis, the leading cause of morbidity and mortality worldwide, is an inflammatory disease characterized by lipid accumulation along the arterial walls. During an immune response, leukocytes and lymphocytes target invading microorganisms,