Foam cells eventually die and further propagate the inflammatory process
The monocytes differentiate into macrophages, which proliferate locally, ingest oxidized LDL, slowly turning into large "foam cells"
Arteriosclerosis - artery becomes thicker and harder
Macrophages die when eating too much
Cytokines recruit more monocytes
Atherosclerosis - hardening of any artery
New smooth muscle secretes collagen and elastin fibrous cells
Plaque - fatty streak and the wall (fibrous cap)
New plaque prevents high-density lipoproteins to remove calcium from the vessel
Fatty streak - build up of foam cells (lesion)
Deposits of calcium into the plaque stiffens the walls of the arteries
A wall is formed around the fatty streak when the new smooth muscle grows
The new wall helps prevent blood clots
Monocytes continue to die while eating low-density lipoprotein
Fatty streaks cause calcium to deposit into the plaque
Dead macrophages - foam cells
Fatty streak allows blood to clot on it
White blood cells break down low-density lipoproteins through oxidation
Platelets gather at the damaged endothelium
Low-density lipoproteins can enter the endothelial wall when endothelium is damaged
White blood cells are called monocytes
Crystals - deposits of calcium into the plaque
Arteriosclerosis - artery is less elastic
Dead macrophages left under the damaged endothelium
Platelets release platelet-derived growth factor
White blood cells break down low-density lipoproteins
Calcium is deposited into the vessel wall by low-density-lipoproteins
Cytokines released when macrophages die
The new wall is a fibrous cap
Platelet-derived growth factor stimulates the growth of smooth muscle cells.
