Modification of low-density lipoproteins by low molecular weight carbonyl products of free-radical oxidation of lipids and carbohydrates plays a key role in atherosclerotic lesion of the vascular wall and in endothelial dysfunction

Q4 Immunology and Microbiology
V. Lankin, A. Tikhaze, V. Y. Kosach, G. Konovalova, A. V. Kudryashova
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引用次数: 0

Abstract

The review presents evidence of the participation of low-density lipoproteins (LDL) modified by low molecular weight dicarbonyl compounds formed during freeradical oxidation of lipids (malondialdehyde) and carbohydrates in the development of endothelial dysfunction and atherosclerotic vascular lesions. The authors believe that it is they, and not oxidized (hydroperoxide-containing) LDL, that are the main factors of pathogenesis. The role of dicarbonyl-modified LDL in LOX-1 dependent induction of processes leading to the development of endothelial dysfunction is discussed. The results of studies proving that damage to the glycocalyx (a layer of macromolecules that prevent the development of endothelial dysfunction) covering the luminal surface of the endothelium is caused by hyperproduction of reactive oxygen species. Ways of pharmacological correction of free-radical oxidation processes are discussed, due to which inhibition of atherogenesis and diabetogenesis can be achieved.
脂质和碳水化合物自由基氧化的低分子量羰基产物对低密度脂蛋白的修饰在血管壁的动脉粥样硬化损伤和内皮功能障碍中起关键作用
该综述提出了低密度脂蛋白(LDL)在脂质(丙二醛)和碳水化合物自由基氧化过程中形成的低分子量二羰基化合物修饰的证据,这些低密度脂蛋白参与了内皮功能障碍和动脉粥样硬化性血管病变的发展。作者认为,这是他们,而不是氧化(含氢过氧化物)LDL,是发病的主要因素。讨论了二羰基修饰LDL在LOX-1依赖性诱导过程中导致内皮功能障碍的作用。研究结果证明覆盖内皮管腔表面的糖萼(一层防止内皮功能障碍发展的大分子)的损伤是由活性氧的过量产生引起的。讨论了自由基氧化过程的药理学纠正方法,从而抑制动脉粥样硬化和糖尿病的发生。
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来源期刊
Acta Biomedica Scientifica
Acta Biomedica Scientifica Immunology and Microbiology-General Immunology and Microbiology
CiteScore
0.40
自引率
0.00%
发文量
106
审稿时长
7 weeks
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