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.
Key words: Coronary artery Disease (CAD), Statins, Endothelium, Caveolin.
Coronary artery disease (CAD) is the most common type of multifactorial chronic heart disease. It is a consequence of plaque buildup in coronary arteries. The arterial blood vessels, which begin out smooth and elastic become narrow and rigid, curtailing blood flow resulting in deprived of oxygen and nutrients to the heart [1].
CAD is a leading cause of morbidity and mortality throughout the worldwide. The prevalence of biological and metabolic risk factors were also found to be high in development of coronary artery disease. Patients with hypercholesterolemia are at increased risk to experience cardiovascular events and to die from vascular disease [2]. .Statins, among the most commonly prescribed drugs worldwide, are cholesterol let downing agents used to manage cardiovascular and coronary heart diseases and to treat hypercholesterolemia. Statin’s therapy ...
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...on and forms an inhibitory complex with caveolin-1 leads to decrease in activity of enzyme in the cells. Transcription of Cav-1 gene is regulated by cholesterol responsive elements. Exposure of fibroblast and endothelial cells to free cholesterol and LDL Cholesterol was found to up regulate Cav-1 expression. Ca+2 mobilizing agents cause disinhibiton of e NOS by promoting Ca+2/Calmodulin triggered dissociation of Cav-1.
Statin downregulates Cav-1 in endothelial cells by blocking the cholesterol synthesis, a favorable effect on vascular function may partly mediated by interruption of the e NOS/Cav-1 complex [24].
Conclusion
In summary, accumulating evidence from various research and clinical trials indicates that Statin have pleiotropic effects, and improves the endothelial function through the increase of endogenous production of NO in different pathways.
...ve stress [8] and can help combat many cardiovascular disorders, thus confirming the protective capabilities of nitric oxide. Another one of nitric oxide’s protective capabilities stems from its role as a potent vasodilator, and these vasodilation properties are primarily achieved through the activity of eNOS. eNOS is a membrane bound protein that is classified as a calcium-calmodulin dependent enzyme [13]. At resting concentrations of calcium, eNOS generates low amounts of nitric oxide, however, as intracellular calcium concentration increases, there is a potent enhancement of nitric oxide production by eNOS [13], which then goes on to cause vasodilation to prevent blockage of blood flow. Due to its generally low output, eNOS is largely associated with basal cardiac function, while iNOS is a much higher output enzyme, generating much more nitric oxide than eNOS [5].
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...s to interfere with bonding to the receptors. The final possibility uses CNP, which downregulates the activation in MAP kinase pathways in the chondrocytes (4).
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Cardiovascular disease is currently the leading cause of death in the United States. It is responsible for one in four deaths every year, about 600,000 mortalities. This disease affects men and women, as well as every ethnic group. Coronary artery disease is the most common cardiovascular disease, representing approximately 400,000 deaths per year of the aforementioned 600,000 total deaths from cardiovascular diseases as a whole. In 2010 alone, coronary artery disease cost the United States $108.9 billion for health care services, medication, and lost productivity. These chilling statistics, published every year by the American Medical Association, demonstrate the immediate need for new and innovative ways to prevent, detect, and treat coronary heart disease. This paper will explore the molecular biology behind the disease while explaining the current treatments and prevention that are available today, why they work and what can be done to improve them.
The cell plasma membrane, a bilayer structure composed mainly of phospholipids, is characterized by its fluidity. Membrane fluidity, as well as being affected by lipid and protein composition and temperature (Purdy et al. 2005), is regulated by its cholesterol concentration (Harby 2001, McLaurin 2002). Cholesterol is a special type of lipid, known as a steroid, formed by a polar OH headgroup and a single hydrocarbon tail (Wikipedia 2005, Diwan 2005). Like its fellow membrane lipids, cholesterol arranges itself in the same direction; its polar head is lined up with the polar headgroups of the phospholipid molecules (Spurger 2002). The stiffening and decreasing permeability of the bilayer that results from including cholesterol occurs due to its placement; the short, rigid molecules fit neatly into the gaps between phospholipids left due to the bends in their hydrocarbon tails (Alberts et al. 2004). Increased fluidity of the bilayer is a result of these bends or kinks affecting how closely the phospholipids can pack together (Alberts et al. 2004). Consequently, adding cholesterol molecules into the gaps between them disrupts the close packing of the phospholipids, resulting in the decreased membrane fluidity (Yehuda et al. 2002).
Heart disease describes a range of conditions that affect your heart. Diseases under the heart disease umbrella include blood vessel diseases, heart rhythm problems, and heart defects. The major cause of this is a build-up of fatty plaques in the arteries. Plaque build-up thickens and stiffens the vessel walls, which can inhibit blood flow through the arteries to organs and tissues.
Edrophonium is a competitive inhibitor of acetylcholinesterase (AChE) [1]. AChE is an extrinsic membrane-hound enzyme that functions in the central and peripheral nervous systems. AChE rapidly terminates the ACh receptor-mediated signal transmission by hydrolyzing Ach. Inhibition of AChE results in accumulation of ACh in the synaptic cleft and leads to impeded neurotransmission [2].
Liao, J. K., (2007). Safety and efficacy of statins in Asians. American Journal of Cardiology, 99(3), 410-414. doi: 10.1016/j.amjcard.2006.08.051
Coronary artery disease (CAD) is the number one killer in America, affecting more than 13 million people. CAD occurs when a fatty substance called plaque builds up in the coronary arteries. These arteries disperse oxygen-ric...
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