How does a helpful substance like cholesterol turn deadly?

You probably know that LDL cholesterol is “bad” and that too much of it in your blood puts you at risk of atherosclerosis, hardening of the arteries. A group of Israeli researchers from the Weizmann Institute of Science wanted to understand how cholesterol, a basic component of life, can turn deadly.

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The job of cholesterol is to provide elasticity to the fatty substance that makes up cell membranes. LDL (low-density lipoprotein) cholesterol acts as “packaging” to help cholesterol travel through the blood, and can even clear away molecular cholesterol that settles on blood vessel walls. The trouble seems to begin when crystals of cholesterol form. These are the material of the plaques that form in lesions, causing irreversible damage that leads to atherosclerosis and eventually to the heart disease and stroke that are the leading killers in the Western world. In their research findings published in the Proceedings of the National Academy of Sciences (PNAS), the scientists showed that these harmful cholesterol crystals form in two different ways in immune cells that unwittingly aid in the progression of the disease. A pathological chain of events When levels of LDL in the blood are too high, some of it is deposited on the blood vessel walls. There, the cholesterol undergoes oxidation, making these molecules toxic to the cells lining the blood vessels. When the immune system recognizes an arterial lesion caused by this oxidation process, it sends “Pacman”-like cells called macrophages to “eat up” the harmful material. But macrophages that overeat– meaning they have too much unwanted stuff to clean up — inflate, turn foamy and die. -- More....

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