Abstract
Atherosclerosis is a multicausal disease characterized by the formation of cholesterol-containing plaque in the pronounced intima nearest to the heart’s elastic-type arteries that have high levels of blood circulation. Plaques are formed due to arterial pressure-induced damage to the endothelium in areas of turbulent blood flow. It is found in the majority of the Western population, including young people. This denies the monogenic mechanism of atherogenesis. In 1988, Orekhov et al. and Kawai et al. discovered that the presence of atherogenic (modified, including oxidized ones) LDLs is necessary for atherogenesis. On the basis of our discovery, suggesting that the overloading of enterocytes with lipids could lead to the formation of modified LDLs, we proposed a new hypothesis explaining the main factors of atherogenesis. Indeed, when endothelial cells are damaged and then pass through the G2 phase of their cell cycle they secrete proteins into their basement membrane. This leads to thickening of the basement membrane and increases its affinity to LDL especially for modified ones. When the enterocyte transcytosis pathway is overloaded with fat, very large chylomicrons are formed, which have few sialic acids, circulate in the blood for a long time, undergo oxidation, and can induce the production of autoantibodies. It is the sialic acids that shield the short forks of the polysaccharide chains to which autoantibodies are produced. Here, these data are evaluated from the point of view of our new model.
Highlights
Atherosclerosis is a non-monogenic, diet-related disease characterized by an accumulation of cholesterol in the intima of the human elastic-type arteries and the formation of intimal plaques, namely, bulging intima containing a lot of cholesterol within the foam cells, which originate from macrophages and smooth muscle cells (SMCs)
Multiple entries of endothelial cells into the G2 phase of the cell cycle induces secretion of the multilayered basement membrane which is more prone to low-density lipoproteins (LDL) binding
Chylomicrons are transformed into LDL which circulate in the blood longer and subjected to oxidation
Summary
Atherosclerosis is a non-monogenic, diet-related disease characterized by an accumulation of cholesterol in the intima of the human elastic-type arteries and the formation of intimal plaques, namely, bulging intima containing a lot of cholesterol within the foam cells, which originate from macrophages and smooth muscle cells (SMCs). It is necessary to distinguish atherosclerosis from arteriosclerosis [1] This disease became almost universal because atherosclerosis was found in the majority of the population, including young people. This denies the monogenic mechanism of atherogenesis. 46% of men and 33% of women have fibrous plaques, and by 35–45 years atherosclerotic formations are found in the arteries of the brain. If you remove genetics, the main cause of its development is improper nutrition (see below)
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