Essay on Atherosclerosis is the Hardening of Artery Walls

Essay on Atherosclerosis is the Hardening of Artery Walls

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Involvement of the CHOP (CEBP Homologous Protein) in Atherosclerosis

Atherosclerosis is a medical condition characterized by the hardening and thickening of the arterial walls due to the accumulation of calcium and lipid materials. It is a condition that is recognized as a leading cause of a plethora of cardiovascular disease conditions. These range from strokes to heart attacks. Atherosclerosis often remains asymptomatic until one experiences the aforementioned cardiovascular problems. Through decades of research on this subject from a variety of different levels, it has been determined that the accumulation of fatty materials and maladaptive inflammatory responses in the arteries are major contributors in what leads to the progression of the disorder. Low density lipoproteins promote the accumulation of macrophages in the arteries and this further leads to inflammatory responses and arterial lesions in more advanced stages. The endoplasmic reticulum (ER) has been implicated as playing a major role in the progression of advanced stages of this disorder. There are two types of ER found within the cell, the rough ER and smooth ER. The rough ER contains ribosomes on its exterior and that is where protein synthesis occurs. The smooth ER does not contain ribosomes and plays the role of regulating lipid metabolism. The ER plays the role of properly folding proteins and secreting them to the golgi apparatus for use in other parts of the cell. It consists of a stack of flattened membranes referred to as cisternae. The lumen or cisternal space within the endoplasmic reticulum accounts for about 10% of the cell’s total volume. Within the phospholipid bilayer of this organelle is a major intracellular reservoir for calcium ions, steroid...


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..., the progression of the illness can be slowed. Although ER-stress related CHOP activity does not play a role in the initial stages of atherosclerosis, it leads to plaque progression and instability when expressed in macrophages in more advanced lesions. It has been observed in many experiments done on both humans and mice that a deficiency in CHOP actually reduces the progression of atherosclerosis. It leads to apoptosis in the macrophages by initiating the UPR through a variety of mechanisms. The UPR is something that is initiated only when there is undo ER-stress. The plaque formation and inflammation in arteries are the triggers that cue this stress in the ERs. Novel therapeutic treatments for the disorder are being developed through research that seeks to better understand the exact role of the CHOP proteins and the UPR in the progression of atherosclerosis.

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