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