**Funding**

*Apolipoproteins, Triglycerides and Cholesterol*

lism of triglyceride-rich lipoproteins [24].

into cholesterol incorporate Apo E [25].

entiation of neurons [26].

*3.1.6 Apolipoprotein (a)*

**4. Conclusion**

chylomicrons, VLDL, IDL, and HDL containing Apo E.

incorporated into the lipoprotein composition of Lp(a).

could be a link between atherosclerosis and fibrinolysis [27].

*3.1.5 Apolipoprotein E*

these apolipoproteins transfer to lipoprotein particles rich in triglycerides, namely, chylomicrons and VLDL. Apparently, Apo C plays a significant role in the catabo-

Apolipoprotein E (Apo E) is a protein molecule composed of 229 amino acids, which contains 10% of the amino acid arginine, and is therefore called the "arginine-rich protein" [16]. The main site of its synthesis is the liver, but it is also created in other organs: brain, spleen, lungs, adrenal gland, kidneys, ovaries, muscles. It plays a significant role in the metabolism of various lipoprotein particles:

Apolipoprotein E participates in the reversible transport of excess cholesterol from peripheral tissues into the liver via HDL particles, which when incorporated

Apo E also appears to be involved in reparative responses to tissue damage. An increase in its concentration is found in sites of peripheral nerve damage and regeneration [25]. It has significance in nerve regeneration, growth, and/or differ-

Apolipoprotein (Apo A) is a relatively large molecular weight protein that is

If Apo A is isolated, the rest of Lp(a) in its composition is almost identical to the LDL particle because it has a similar lipid composition and contains a single molecule of Apo B-100. The gene that regulates the synthesis of this apolipoprotein is located on the sixth chromosome near the plasminogen gene. Apo A has a great structural similarity and shows immune cross-reactivity with plasminogen, which

Lipid disorders are of fundamental importance for atherogenesis and even the occurrence of ischemic heart disease and other cardiovascular and cerebrovascular diseases. They are often associated with diabetes, obesity, and hypertension with which they interact synergistically, leading to arteriosclerotic changes. Atherosclerosis is caused by changes in the wall of blood vessels characterized by lipid deposition and cell proliferation. Deposited lipids in the blood vessel wall originate from plasma lipoproteins, and elevated cholesterol, especially LDL cholesterol, is a major risk factor. Atherogenic lipoproteins include, in addition to LDL particles, almost all classes of Apo B-containing lipoproteins (VLDL, VLDL residues, IDL, Lp(a), and oxidized LDL). A common feature of all atherogenic lipoproteins is that they contain different amounts of cholesterol esters and/or Apo B-100 or Apo B-48. Atherogenic effects of triglyceride-rich lipoproteins are associated with postprandial lipemia after fatty meal intake. Atherosclerosis is considered an inevitable process at the present stage of medical science development. In most people, around the age of 85, it is thought that about 60% of coronary circulation is covered by atherosclerotic plaques, provided that no risk factors are present during life. In the presence of risk factors such as hypercholesterolemia, such changes in the coronary vessels are reached sometime in the 42nd year of life. This early atherosclerosis is a global problem for humanity today. The major risk factors for

**8**

None.
