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Reverse cholesterol transport is a multi-step process resulting in the net movement of cholesterol from peripheral tissues back to the liver first via entering the lymphatic system, then the bloodstream. [1] Cholesterol from non-hepatic peripheral tissues is transferred to HDL by the ABCA1 (ATP-binding cassette transporter). [2]
Atherosclerosis [a] is a pattern of the disease arteriosclerosis, [8] characterized by development of abnormalities called lesions in walls of arteries. This is a chronic inflammatory disease involving many different cell types and is driven by elevated levels of cholesterol in the blood. [9]
Several steps in the metabolism of HDL can participate in the transport of cholesterol from lipid-laden macrophages of atherosclerotic arteries, termed foam cells, to the liver for secretion into the bile. This pathway has been termed reverse cholesterol transport and is considered as the classical protective function of HDL toward atherosclerosis.
1071 n/a Ensembl ENSG00000087237 n/a UniProt P11597 n/a RefSeq (mRNA) NM_000078 NM_001286085 n/a RefSeq (protein) NP_000069 NP_001273014 n/a Location (UCSC) Chr 16: 56.96 – 56.98 Mb n/a PubMed search n/a Wikidata View/Edit Human Cholesteryl ester transfer protein (CETP), also called plasma lipid transfer protein, is a plasma protein that facilitates the transport of cholesteryl esters and ...
Drugs in this class substantially increase HDL cholesterol, lower LDL cholesterol, and enhance reverse cholesterol transport. [citation needed]CETP inhibitors inhibit cholesterylester transfer protein (CETP), which normally transfers cholesterol from HDL cholesterol to very low density or low density lipoproteins (VLDL or LDL).
A cardiologist specializes in cardiology, which is the study of your heart and blood vessels. Diagnosing Atherosclerosis. Your doctor may screen you for atherosclerosis during a general check-up ...
This movement of cholesterol is known as reverse cholesterol transport and is a protective mechanism against the development of atherosclerosis, which is the principal cause of heart disease and stroke. SR-BI is crucial in carotenoid and vitamin E uptake in the small intestine.
Downregulation of ABCA1 in senescent macrophages disrupts the cell's ability to remove cholesterol from its cytoplasm, leading the cells to promote pathologic atherogenesis (blood vessel thickening/hardening) which "plays a central role in common age-associated diseases such as atherosclerosis, cancer, and macular degeneration" [20] Knockout ...
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