engleski

The role of modified lipoproteins in atherosclerosis and diabetes

Cardiovascular diseases in general, and atherosclerosis in particular, are the leading causes of morbidity and mortality in the older population and people with diabetes mellitus. The widely accepted risk factors for the development of atherosclerosis are elevated levels of plasma lipoproteins, hypertension and smoking. Epidemiological and experimental studies have provided compelling evidence for this relationship. Recently, increased attention has been focused not only to the elevated plasma lipoproteins, but also to the altered composition of lipid and protein ingredients of lipoproteins. A more focused approach to the role of modified lipoproteins in the pathogenesis of macrovascular disease is consequently analysed in this review. It is now estimated that several modified forms of lipoproteins are involved in many of the biological events associated with development and progression of atherosclerosis. In atherogenesis, lipoprotein modifications with marked atherogenic potential include oxidized lipoproteins, glycated lipoproteins, lipoprotein immune complexes and compositional changes like small dense LDL or triglyceride-rich lipoproteins. Modifications such as oxidation and glycation change the recognition status of LDL by the LDL-receptor. Thus, LDL in their modified form are not recognized by the LDL-receptor, but are taken up by arterial wall cells, especially by macrophages, through the so-called scavenger-receptor pathway. As a result of this uptake, vascular wall macrophages may become transformed into lipid-laden "foam" cells that presage the development of fatty streaks and the complex, proliferative lesions of atherosclerotic plaque. In this review it will be discussed how modification of lipoproteins and alterations in lipoprotein composition alter their function and can contribute to the accelerated development of macrovascular disease.

Oxidized lipoproteins; Lipoproteine immune complexes; Lipoprotein glycation; Small dense LDL

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