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The review deals with modern data on the hepatic lipase (HL) role in the atherosclerosis development. HL enzyme facilitates the TG output from the pool of the very low density lipoproteins (VLDL), and this function is controlled by the high-density lipoprotein (HDL) particles composition and structure. The composition of HDL regulates the “liberation” of the HL from the liver, and the structure of HDL controls the HL transportation and activation of it in the bloodstream. Although the lipase activity is typically hard to detect in human plasma, heparin infusion increases the mass of HL and stimulates their activity in the circulation. In humans, the HL can be found primarily in association with the hepatocytes and endothelial cells of the liver cell surface. Human HL can be released from the HSPG cell surface via either heparin or HDL. Some results suggest that heparin interacts directly with lipases and/or competes for binding sites on the surface of HSPG cells. Increased levels of apolipoprotein B-containing lipoproteins (Apo-containing lipoproteins), LDL, and chylomicrons are connected with the development of atherosclerosis. Deposition of lipids in monocytes and macrophages leads to the further development of atherosclerosis. In general, these results indicate that dyslipidemia caused by deficiency HL in combination with a diet high in cholesterol causes inflammation of the liver steatosis.

The decisive role of the hepatic lipase in the reverse cholesterol transport