Once again in defense of cholesterol
Russian biologists have revealed the true cause of atherosclerosis
Blood vessels begin to overgrow with cholesterol plaques and lose flexibility not because of disorders in fat metabolism, but because of the development of foci of inflammation. This conclusion was reached by Russian and foreign doctors who published their findings in the journals Atherosclerosis and Current Pharmaceutical Design.
"Surprisingly, none of the ten genes we discovered were associated with cholesterol metabolism. This indicates that activation of pro–inflammatory genes plays a key role here, whereas changes in the work of genes associated with fat metabolism can be initiated by inflammation itself," explains Alexander Orekhov from the Research Institute of General Pathology and Pathophysiology of the Russian Academy of Sciences in Moscow.
The Invisible Killer
Atherosclerosis and concomitant heart and vascular diseases, according to WHO statistics, remain one of the main causes of death in most countries of the world. As a rule, the development of this disease begins with the accumulation of cholesterol on the walls of blood vessels, which after a while leads to their thickening, accumulation of calcium in them and loss of flexibility.
So far, scientists have not revealed the specific mechanisms of the formation of cholesterol plaques and calcareous deposits in the walls of blood vessels. Some researchers believe that changes in the work of genes associated with fat metabolism, leading to the accumulation of "harmful" cholesterol in the blood, are to blame for the development of atherosclerosis. Other biologists suggest that the "trigger" of the disease is something else.
According to the press service of the Russian Scientific Foundation, which supported the research of Professor Orekhov and his colleagues, Russian doctors, as well as their Japanese, American and German colleagues, managed to get closer to revealing the true causes of the development of this disease.
Scientists have drawn attention to the fact that not only the fat molecules themselves are involved in the formation of cholesterol plaques, but also their two potential "accomplices" – macrophages, immune system cells living on the walls of blood vessels, as well as special proteins, the so-called low-density lipoproteins.
Both cells and proteins are involved in the process of removing excess fat from the bloodstream. Lipoproteins "collect" cholesterol and other fat molecules into peculiar lumps, most of which enter the liver, and the rest are eaten by macrophages.
Protein "fifth column"
As scientists believe today, disorders in fat metabolism lead to the fact that the structure of lipoproteins changes abnormally, and they begin not to disintegrate, but to accumulate inside macrophages, which gradually kills them and leads to the formation of fat deposits inside the walls of blood vessels.
Orekhov and his colleagues checked whether this was really the case by preparing a special version of lipoproteins, which are almost guaranteed to cause atherosclerosis, and watching how their ingestion into macrophages would change the work of their genes.
The ingestion of such structures into cells really caused them to accumulate cholesterol, but not at all for the reason indicated by the generally accepted theories of the development of atherosclerosis.
It turned out that it was not the genes associated with fat metabolism that changed the most and first of all, but the DNA sections that control the work of the immune system. Almost all of them, for example, the genes CXCL8, F2RL1 and IL15, contribute to the development of inflammation and related processes.
This suggests that high cholesterol and lipoproteins alone do not provoke atherosclerosis. Inflammatory processes were "to blame" for this, somehow changing how macrophages and other immune cells interact with fats.
Accordingly, suppressing inflammation may be the most effective way to prevent or slow down the development of atherosclerosis. Doctors hope to test this idea in the near future.
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