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Apolipoproteins and amyloid fibril formation in atherosclerosis

机译:动脉粥样硬化中载脂蛋白和淀粉样蛋白原纤维的形成

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摘要

Amyloid fibrils arise from the aggregation of misfolded proteins into highly-ordered structures. The accumulation of these fibrils along with some non-fibrillar constituents within amyloid plaques is associated with the pathogenesis of several human degenerative diseases. A number of plasma apolipoproteins, including apolipoprotein (apo) A-I, apoA-II, apoC-II and apoE are implicated in amyloid formation or influence amyloid formation by other proteins. We review present knowledge of amyloid formation by apolipoproteins in disease, with particular focus on atherosclerosis. Further insights into the molecular mechanisms underlying their amyloidogenic propensity are obtained from in vitro studies which describe factors affecting apolipoprotein amyloid fibril formation and interactions. Additionally, we outline the evidence that amyloid fibril formation by apolipoproteins might play a role in the development and progression of atherosclerosis, and highlight possible molecular mechanisms that could contribute to the pathogenesis of this disease.
机译:淀粉样蛋白原纤维是由错误折叠的蛋白质聚集成高度有序的结构而产生的。这些原纤维以及一些非原纤维成分在淀粉样蛋白斑块中的积累与几种人类变性疾病的发病机理有关。许多血浆载脂蛋白,包括载脂蛋白(apo)A-I,apoA-II,apoC-II和apoE与淀粉样蛋白形成有关,或受其他蛋白影响淀粉样蛋白形成。我们回顾了目前载脂蛋白在疾病中淀粉样蛋白形成的知识,尤其是动脉粥样硬化。可从体外研究中进一步了解其淀粉样蛋白生成倾向的分子机制,这些研究描述了影响载脂蛋白淀粉样蛋白原纤维形成和相互作用的因素。此外,我们概述了载脂蛋白形成淀粉样蛋白原纤维可能在动脉粥样硬化的发生和发展中起作用的证据,并重点介绍了可能导致该病发病机理的分子机制。

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