Foam cells eventually die, and further propagate the inflammatory process.

Foam cells are the body's way of trying to get rid of bad cholesterol from the blood vessels.

If foam cells are present, standard treatments for atherosclerosis are an appropriate treatment.

Foam cells and apocrine cells may also be seen, although these are less diagnostic features.

In Germany he became the first to describe the cholesterinesterphagozyten, which derive from macrophages and today are known as foam cells.

The foam cells thus created also make the material quite buoyant, and the diver must compensate for this by wearing weights.

Macrophages accumulate modified lipid particles and become foam cells.

Foam cells do not give off any explicit signs or symptoms, but they are part of the origin of atherosclerosis.

Foam Cells are lipid-loaded macrophages that have surrounded large amounts of a fatty substance, usually cholesterol.

Foam cells are formed when the body sends macrophages to the location of a fatty deposit on the blood vessel walls.

Foam cells are not dangerous as such, but can become a problem when they accumulate at particular foci thus creating a necrotic centre of atherosclerosis.

Dehydroepiandrosterone, an adrenal androgen, increases human foam cell formation: a potentially pro-atherogenic effect.

After they accumulate large amounts of cytoplasmic membranes (with associated high cholesterol content) they are called foam cells.

Low-density lipoprotein (LDL) cholesterol is contained by a foam cell.

Foam cells characterize atherosclerotic lesions.

Atherosclerosis is marked by an excessive accumulation of cholesterol by macrophages, leading to their transformation into foam cells.

The formation of foam cells and their continued accumulation in the intima lead to the formation of fatty streaks.

Scavenger receptors typically are found on macrophages, with cholesterol laden macrophages being better known as "foam cells".

Foam cells are tiny in size and can only be truly detected by examining a fatty plaque under a microscope after it is removed from the body.

ANGPTL4 suppresses foam cell formation to reduce atherosclerosis development.

Instead CXCL5 has a protective role in atherosclerosis by directly controlling macrophage foam cell formation.

The oxidized LDL accumulates in the macrophages and other phagocytes, which are then known as foam cells.

They are cutaneous manifestations of lipidosis in which there is an accumulation of lipids in large foam cells within the skin.

Atherosclerosis is caused by the accumulation of macrophages containing cholesterol (foam cells) in artery walls (in the intima).

They can be found in trace amounts in every cell type but are highly enriched in foam cells and are common components of human skin oil.