Various conditions, like high concentrations of Low Density Lipoproteins (LDL), Free radicals, Hypertension, Diabetes and others, can damage vascular endothelium and begin the formation of a pathological accumulation of Cholesterol.
The atheromatose lesion or plaque that is formed represents an inflammatory rather than a simple deposition of cholesterol: LDL can seep through the endothelium and interact with proteoglycans, and being deposited in the subendothelial space. Macrophages that accumulate in the lession fagocyte LDL and become “foam cells”. Smooth muscle cells can also migrate to the subendothelial space and become foam cells. The plaque continue growing and begins to occlude the blood vessel, causing tissue ischemia or infarction. When the foam cells die, they release toxic substances that contribute to the plaque rupture and the formation of blood clots and thrombi.
This clip shows an interesting animation representing the formation of the plaques.
High Density Lipoproteins (HDL) will help to eliminate the plaque cholesterol. HDL can capture the cholesterol deposited in the plaques, through the mechanisms described when HDL functions were discussed: esterification of cholesterol as a result of the action of LCAT, followed by solubilization of the cholesterol esters in the HDL core, transportation of cholesterol to the liver, and excretion from the liver mainly as bile salts.
The term “Bad Cholesterol” is used for the LDLc (LDL associated cholesterol), since it is the cholesterol that is transported from the liver to the peripheral tissues, and has the potential to be deposited in arteries, while the term “Good Cholesterol” is used for the HDL associated Cholesterol, since it is Cholesterol that is being transported from peripheral tissues to the liver, where it is going to be eliminated in bile as cholesterol or by its conversion to bile salts.
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