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Page 2 of 6 Sobenin. Vessel Plus 2020;4:18 I http://dx.doi.org/10.20517/2574-1209.2020.09

Figure 1. Current concepts of atherogenesis: schematic outline of key events and unresolved issues. LDL: low density lipoprotein; VLDL:
very low density lipoprotein; Lp(a): lipoprotein (a)

the last few decades, progress in the reduction of cardiovascular mortality has been achieved mainly
due to successful cardiovascular surgery and healthier lifestyles, which suggests that the battle against
atherosclerotic disease has been won. However, the reduced role of cardiovascular disease in overall
mortality is observed only in several developed countries. Globally however, atherosclerosis and related
diseases still remain as one of the leading causes of mortality. It is true that patients have gained additional
years of life from surgery and lipid-lowering medications, but did the underlying atherosclerosis resolve?
Have the cellular and molecular mechanisms of atherogenesis been altered? Was there progress in the
development of new strategies in anti-atherosclerotic treatment? No. Thus, it is time to discuss both the
novel and debatable aspects of atherosclerosis and atherogenesis, with due consideration for the latest
developments in molecular and cellular biology in vascular medicine.

Atherosclerosis can generally be described as an excessive fibro-fatty, proliferative and inflammatory
response to arterial wall damage and involves several cell types such as monocyte-derived macrophages,
[1,2]
smooth muscle cells, dendritic cells, lymphocytes and platelets . It is well known that at the level of the
arterial wall, the deposition of intracellular cholesterol and foam cell formation are the typical features of
[3,4]
early atherosclerosis . Current understanding of the development of early atherosclerotic lesions is shown
in Figure 1. In brief, circulating lipoproteins - low density lipoprotein (LDL), the remnants of very low
density lipoproteins (VLDL remnants) and lipoprotein(a) - serve as sources of lipids which can accumulate
[4-8]
further in the arterial wall . After penetrating the subendothelial intima, lipoproteins may induce lipid