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High cholesterol does not lead to heart disease
Last reviewed: 01.07.2025
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Atherosclerosis is the main cause of fatal cardiovascular diseases.
The theory that high cholesterol is a major risk factor for strokes and heart attacks has been around for a long time and has fueled debate among researchers, half of whom support this hypothesis and the other half refute it.
Although high blood cholesterol is considered a dangerous symptom, some experts question the advisability of treating patients with statins, drugs that lower cholesterol.
Researchers at the University of California and their colleagues from other American institutes claim that cholesterol precursors actually suppress inflammatory reactions in the body. A precursor is an auxiliary substance that participates in reactions that lead to the creation of a target substance, in this case cholesterol. These precursors could be the target of research to create drugs to combat atherosclerosis, which kills thousands of people every year.
The walls of the arteries contain immune system cells called macrophages. They are responsible for detecting and neutralizing foreign cells or matter that may pose a threat to the body.
As Christopher Glass, a professor at the University of California's School of Medicine, explains, these macrophages are able to effectively destroy excess cholesterol.
But some macrophages, instead of neutralizing excess cholesterol, are themselves transformed under its influence into xanthomatous macrophage cells.
These xanthomatous macrophage cells recruit other immune cells and produce molecules that trigger certain genes to trigger inflammatory responses.
For a long time it was believed that it was the appearance of these cells in the walls of the arteries that led to the accumulation of cholesterol and inflammatory processes.
But Glass and his colleagues wanted to track this process precisely and find out why individual macrophages were failing to perform their function. During their research, the scientists made two unexpected discoveries.
"Firstly, the xanthomatous macrophage cells suppress the activity of genes that trigger inflammatory responses in the body, although previously we thought that everything happens the other way around," Professor Glass explained. "Secondly, we identified a molecule that helps normal macrophages control cholesterol balance. When there are enough of these molecules, they destroy excess cholesterol and prevent the production of new cholesterol."
This molecule is desmosterol, the final precursor in the creation of cholesterol. Desmosterol is produced by cells and used as a structural component of their membranes. Researchers believe that atherosclerotic lesions disrupt the normal function of this molecule.
Now the new task for scientists is to study desmosterol in depth in order to find out the reasons why their normal activity is disrupted.
"We have learned a lot over the last 50 years. We may now be on the way to creating a new drug that can control cholesterol balance without the side effects," hopes Professor Glass.
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