Cardiac dysfunction and oxidative stress in the metabolic syndrome: an update on antioxidant therapies.
Cardiac dysfunction and oxidative stress in the metabolic syndrome: an update on antioxidant therapies.
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DOI：
10.2174/1381612811319270003
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发表时间：
2013
影响因子：
3.1
通讯作者：
Boudina S
中科院分区：
文献类型：
--
作者：
Ilkun O;Boudina S
代谢综合征（MetS）是一组危险因素，包括肥胖、胰岛素抵抗、血脂异常、血压升高和葡萄糖耐受不良。MetS增加了患心血管疾病（CVD）和2型糖尿病的风险。代谢当量的每个组成部分都会导致心功能障碍，它们的组合会带来额外的风险。MetS中心功能障碍的机制是复杂的，可能包括脂质积累、纤维化和硬度增加、钙稳态改变、自噬异常、底物利用改变、线粒体功能障碍和氧化应激增加。线粒体和线粒体外活性氧（ROS）来源和抗氧化防御机制的降低是MetS患者心肌的特征。MetS中心脏氧化应激增加的机制尚不完全清楚，但包括脂肪酸氧化增加，线粒体功能障碍和NADPH氧化酶活性增强。旨在减少氧化应激和增强抗氧化防御的疗法已被用于减少动物met的心功能障碍。相比之下，由于缺乏疗效和不良副作用，使用抗氧化剂治疗心血管疾病的大规模临床试验令人失望。这篇综述的重点是总结目前关于MetS中心脏功能障碍机制的知识，并特别关注氧化应激的作用。最后，我们将向读者更新天然抗氧化剂和线粒体靶向抗氧化剂治疗MetS中CVD的结果。
The metabolic syndrome (MetS) is a cluster of risk factors including obesity, insulin resistance, dyslipidemia, elevated blood pressure and glucose intolerance. The MetS increases the risk for cardiovascular disease (CVD) and type 2 diabetes. Each component of the MetS causes cardiac dysfunction and their combination carries additional risk. The mechanisms underlying cardiac dysfunction in the MetS are complex and might include lipid accumulation, increased fibrosis and stiffness, altered calcium homeostasis, abnormal autophagy, altered substrate utilization, mitochondrial dysfunction and increased oxidative stress. Mitochondrial and extra-mitochondrial sources of reactive oxygen species (ROS) and reduced antioxidant defense mechanisms characterize the myocardium of humans and animals with the MetS. The mechanisms for increased cardiac oxidative stress in the MetS are not fully understood but include increased fatty acid oxidation, mitochondrial dysfunction and enhanced NADPH oxidase activity. Therapies aimed to reduce oxidative stress and enhance antioxidant defense have been employed to reduce cardiac dysfunction in the MetS in animals. In contrast, large scale clinical trials using antioxidants therapies for the treatment of CVD have been disappointing because of the lack of efficacy and undesired side effects. The focus of this review is to summarize the current knowledge about the mechanisms underlying cardiac dysfunction in the MetS with a special interest in the role of oxidative stress. Finally, we will update the reader on the results obtained with natural antioxidant and mitochondria-targeted antioxidant therapies for the treatment of CVD in the MetS.
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