Study Finds New Approach to Unclogging Arteries
By Maggie Fox, Health and Science Correspondent Saturday, August 16, 2003
Washington (Reuters) - U.S. researchers said they had found a key mechanism involved when
cholesterol clogs arteries, and said it may open up a whole new way to treat and prevent heart
attacks and stroke.
Drugs first developed 40 years ago, and then abandoned, could help prevent clots from breaking off
and clogging the artery, they report.
When people have too much cholesterol in their blood, immune cells called macrophages seize fatty
particles and try to drag them out through the walls of the artery. But they are too big, get stuck
and eventually the macrophages die.
These plugs of dead cells are what causes atherosclerosis -- the hardening and clogging of
the arteries.
In two papers published in the Proceedings of the National Academy of Sciences and Nature Cell
Biology this week, Dr. Ira Tabas of Columbia University in New York and colleagues showed they had
found the mechanism that kills the cells, and a drug that may stop the process.
"In order to get atherosclerosis, you need two things going on -- you need high levels of LDL (low-
density lipoprotein or 'bad' cholesterol) in the blood and you need events going in the arterial
wall," Tabas said in a telephone interview.
"Statins are utterly fantastic at lowering LDL," he said. But they only lower the risk of stroke or
heart attack by about 30 percent.
Tabas believes a drug that could stop the macrophages from dying and clogging up the arteries in the
first place would work in tandem with statins and similar drugs to prevent heart disease.
MESSING UP THE PROTEINS
When a macrophage gobbles up a piece of cholesterol, it is moved to an organelle inside the cell
called the endoplasmic reticulum. This is the machine responsible for making the cell's proteins,
and making proteins is what cells must do to survive and function. . . . [...] This is only an
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