Abstract
It has been suggested that low density lipoprotein-containing circulating immune complexes (LDL-CIC) play a role in atherogenesis and are involved in the formation of early atherosclerotic lesion. These complexes, as well as anti-LDL autoantibodies, have been found in the blood and in the atherosclerotic lesions of patients with different cardiovascular diseases, as well as in the blood of animals with experimental atherosclerosis. It can be suggested that the presence of anti-LDL antibodies in the blood is a result of immune response induced by lipoprotein modification. LDL-CIC differs from native LDL in many aspects. It has much lower sialic acid content, smaller diameter, and higher density and is more electronegative than native LDL. Fraction of LDL-CICs is fundamental to the serum atherogenicity manifested at the cellular level. LDL-CIC, unlike native LDL, is able to induce intracellular accumulation of neutral lipids, especially esterified cholesterol, in cells cultured from uninvolved human aortic intima and in macrophage cultures. After removal of LDL-CIC, the CHD patient's sera lose their atherogenic properties. Titer of LDL-CIC in blood serum significantly correlates with progression of atherosclerosis in human in vivo and has the highest diagnostic value among other measured serum lipid parameters. Elevated CIC-cholesterol might well be a possible risk factor of coronary atherosclerosis.
Highlights
Spread clinical manifestations of atherosclerosis such as coronary heart disease (CHD), cerebrovascular stroke, renovascular hypertension, and violation of the lower limbs vascular permeability, are the result of formation of advanced atherosclerotic lesions in a vascular wall
On the basis of current data, it is possible to define the role of lipoprotein-containing immune complexes in atherogenesis (Figure 1)
Atherogenic modified low density lipoprotein (LDL) triggers the production of anti-LDL autoantibodies which react with LDL, leading to the formation of an LDL-containing immune complex
Summary
Spread clinical manifestations of atherosclerosis such as coronary heart disease (CHD), cerebrovascular stroke, renovascular hypertension, and violation of the lower limbs vascular permeability, are the result of formation of advanced atherosclerotic lesions in a vascular wall. A trigger mechanism for the development of atherosclerotic lesions is an intracellular lipid deposition and subsequent foam cell formation with excessive production of connective tissue matrix components and, possibly, cellular proliferation and inflammatory reactions [1, 2]. Atherosclerosis can be generally described as an excessive fibrofatty, proliferative, inflammatory response to damage of the artery wall, involving several cell types, such as smooth muscle cells, monocyte-derived macrophages, lymphocytes, and platelets [3]. During the last three decades, the autoimmune hypothesis of atherosclerosis was developed and the evidence for an important role for autoantibodies against modified low density lipoprotein (LDL) and LDL-containing circulating immune complexes (LDL-CIC) in atherogenesis has been accumulated. Immunological factors appear to contribute to the development of atherosclerosis as many other factors including alterations in plasma lipid and lipoprotein levels, platelet function, BioMed Research International clotting factors, arterial smooth muscle cell metabolism, and blood pressure regulation. The atherogenic properties of LDLcontaining immune complexes suggest them as a candidate marker for atherosclerosis
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