ATHEROSCLEROSIS

It is believed that atherosclerosis is caused by a response to damage to the arterial endothelium which can result from high cholesterol levels, high blood pressure, and cigarette smoking (What). When there is damage to the arterial wall, an inflammatory response occurs and monocytes enter the arterial wall, becoming macrophages in the tissue. These macrophages ingest oxidized cholesterol, becoming foam cells, so called because of the numerous vesicles of lipid they contain. These give the appearance of fatty streaks in the vessel wall. The foam cells die out and the inflammatory response continues, with intracellular microcalcification of the smooth muscle cells adjacent to the atheroma. As cells die, extracellular calcium depo

. . .
o retain antiatherogenic properties without also raising triglycerides. Cholesterol 7?-hydroxylase (CYP7A1) is the rate-limiting enzyme in the pathway that converts cholesterol to bile acids (Zhang and Mangelsdorf). LXR-? regulates gene expression of CYP7A1. It upregulates the transcription of CYP7A1 by directly binding to LXRE in the promoter region of this gene. The bile receptor farnesoid X receptor (FXR) binds bile acids and induces the expression of small heterodimer partner (SHP), an orphan nuclear receptor that preferentially dimerizes with liver receptor homolog 1 (LHR-1) and represses several enterohepatic genes involved in the synthesis and transport of bile acids, including CYP7A1. LXR and FXR thus act as opposing factors in bile acid metabolism, operating together to tightly regulate bile acid homeostasis. LXR functions with a cholesterol precursor and FXR functions with a cholesterol metabolite to up- and downregulate CYP7A1. In the small intestine, at least three ABC transporters are transcriptionally regulated by LXRs and limit cholesterol absorption by pumping it back into the lumen of the gut (Zhang and Mangelsdorf). ABCA1 is upregulated by LXRs in both the intestine and macrophage foam cells. In ma
. . .

Some common words found in the essay are:
Introduction Atherosclerosis, Atherosclerosis Macrophages, PPAR- PPAR-, Li Glass, ABCA1 ABCG1, Dean ABC, Mangelsdorf LXRs, Gene ABCA1, Glass Studies, LXR- THP-1, et al, cholesterol efflux, foam cells, cholesterol transport, reverse cholesterol, reverse cholesterol transport, zhang mangelsdorf, li glass, 26 june 2005, 26 june, june 2005, gene expression, chinetti et al, cholesterol efflux macrophages, nagappa vijay ramprasad,
Approximate Word count = 8856
Approximate Pages = 35 (250 words per page)