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非酒精性脂肪性肝病 (NAFLD) 与心血管疾病之间关系的病理生理机制和临床证据。

Pathophysiological mechanisms and clinical evidence of relationship between Nonalcoholic fatty liver disease (NAFLD) and cardiovascular disease.

机构信息

Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, I-80138 Naples, Italy.

Department of Translational Medical Sciences, University of Campania Luigi Vanvitelli, I-80138 Naples, Italy.

出版信息

Rev Cardiovasc Med. 2021 Sep 24;22(3):755-768. doi: 10.31083/j.rcm2203082.

Abstract

Evidence suggests a close connection between Nonalcoholic Fatty Liver Disease (NAFLD) and increased cardiovascular (CV) risk. Several cross-sectional studies report that NAFLD is related to preclinical atherosclerotic damage, and to coronary, cerebral and peripheral vascular events. Similar results have been showed by prospective studies and also by meta-analyzes on observational studies. The pathophysiological mechanisms of NAFLD are related to insulin resistance, which causes a dysfunction in adipokine production, especially adiponectin, from adipose tissue. A proinflammatory state and an increase in oxidative stress, due to increased reacting oxygen species (ROS) formation with consequent oxidation of free fatty acids and increased de novo lipogenesis with accumulation of triglycerides, are observed. These mechanisms may have an impact on atherosclerotic plaque formation and progression, and they can lead to increased cardiovascular risk in subjects with NAFLD. This review extensively discusses and comments current and developing NAFLD therapies and their possible impact on cardiovascular outcome.

摘要

有证据表明,非酒精性脂肪性肝病(NAFLD)与心血管(CV)风险增加密切相关。几项横断面研究报告称,NAFLD 与临床前动脉粥样硬化损伤以及冠状动脉、脑和外周血管事件有关。前瞻性研究和对观察性研究的荟萃分析也得出了类似的结果。NAFLD 的病理生理机制与胰岛素抵抗有关,后者导致脂肪组织中脂联素等 adipokine 产生功能障碍。由于增加了活性氧(ROS)的形成,导致游离脂肪酸的氧化增加,以及新的脂肪生成增加和甘油三酯的积累,会出现促炎状态和氧化应激增加。这些机制可能对动脉粥样硬化斑块的形成和进展有影响,并可能导致 NAFLD 患者的心血管风险增加。这篇综述广泛讨论和评论了当前和正在开发的 NAFLD 治疗方法及其对心血管结局的可能影响。

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