代谢综合征血管损伤的分子机制。

S Yamagishi, K Nakamura, Y Jinnouchi, K Takenaka, T Imaizumi
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引用次数: 0

摘要

代谢综合征与胰岛素抵抗密切相关,已被认为是内脏型肥胖、高血压、糖尿病和血脂异常等心血管疾病的一组危险因素。最近,在没有明显糖尿病或代谢综合征的情况下,胰岛素抵抗已被证明与内皮功能障碍有关,内皮功能障碍是动脉粥样硬化过程的初始步骤之一。在本文中,我们回顾了代谢综合征引起内皮功能障碍并随后促进动脉粥样硬化的分子机制。我们还讨论了有希望的治疗策略,专门针对代谢综合征中血管改变的机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Molecular mechanisms for vascular injury in the metabolic syndrome.

The metabolic syndrome is strongly associated with insulin resistance and has been recognized as a cluster of risk factors for cardiovascular diseases such as visceral obesity, hypertension, diabetes and dyslipidemia. Recently, insulin resistance in the absence of overt diabetes or the metabolic syndrome itself has been shown to be associated with endothelial dysfunction, one of the initial steps in the process of atherosclerosis. In the present article we review the molecular mechanisms by which the metabolic syndrome causes endothelial dysfunction and subsequently promotes atherosclerosis. We also discuss promising therapeutic strategies that specifically target the mechanisms responsible for vascular alterations in the metabolic syndrome.

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