Rodriguez had already observed how HDL pulls cholesterol out
of foam cells, which are found in the plaque that accumulates on blood vessel walls in people with atherosclerosis.
«We would
take foam cell [models] and make them chock full of cholesterol, put HDL outside the cell, and see how well cholesterol was moving out of the cell — the more HDL the better,» Rodriguez recalls.
The only other one that comes to mind is the SENS foundation's development of an enzyme for removing oxidized cholesterol
from foam cells.
Western - type diets containing moderately high levels of SF (~ 35 kcal % fat,), as (cocoa butter, palm oil, or dairy butter), cholesterol (~ 0.5 to 1 % w / w) and cholic acid (~ 0.1 % to 0.5 % w / w), are capable of inducing elevations in TC and LDL - C and mild atherosclerosis (i.e. cholesterol
laden foam cells, fatty deposits or streaks) in some mouse strains after 12 weeks (14 - 16).
Atherosclerosis is initiated by high plasma cholesterol leading to monocyte entry into the artery wall and differentiation into macrophages, which take up lipoprotein cholesterol to become lipid
engorged foam cells.
Over time, these white blood cells, known
as foam cells, begin to invade the linings of arteries, causing further arterial damage and obstructing blood flow.
Effects of conjugated linoleic acid isomers on monocyte, macrophage and
foam cell phenotype in atherosclerosis.
The insulin causes the initial injury to the vessel wall, then the cascade of events ie macrophages ingesting LDL particles,
foam cells etc are secondary reactions.
The longer cholesterol stays high the more prone it is to oxidisation, the more oxidised it becomes the greater the propensity to
induce foam cell production and arterial occlusion as a result of inflammation.
If the oxLDL / LOX -1 internalization occurs in a monocyte, the macrophage is phenotypically transformed into the classic «
foam cell», which is the sine qua non of atherosclerosis.