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Mitochondrial Dysfunction in Metabolic Syndrome and Asthma

机译:代谢综合征和哮喘的线粒体功能障碍

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Though severe or refractory asthma merely affects less than 10% of asthma population, it consumes significant health resources and contributes significant morbidity and mortality. Severe asthma does not fell in the routine definition of asthma and requires alternative treatment strategies. It has been observed that asthma severity increases with higher body mass index. The obese-asthmatics, in general, have the features of metabolic syndrome and are progressively causing a significant burden for both developed and developing countries thanks to the westernization of the world. As most of the features of metabolic syndrome seem to be originated from central obesity, the underlying mechanisms for metabolic syndrome could help us to understand the pathobiology of obese-asthma condition. While mitochondrial dysfunction is the common factor for most of the risk factors of metabolic syndrome, such as central obesity, dyslipidemia, hypertension, insulin resistance, and type 2 diabetes, the involvement of mitochondria in obese-asthma pathogenesis seems to be important as mitochondrial dysfunction has recently been shown to be involved in airway epithelial injury and asthma pathogenesis. This review discusses current understanding of the overlapping features between metabolic syndrome and asthma in relation to mitochondrial structural and functional alterations with an aim to uncover mechanisms for obese-asthma.
机译:尽管严重或难治性哮喘仅影响不到10%的哮喘人口,但它消耗了大量的健康资源,并导致明显的发病率和死亡率。重度哮喘并没有落在哮喘的常规定义中,需要其他治疗策略。已经观察到哮喘严重程度随较高的体重指数而增加。一般而言,肥胖哮喘患者具有代谢综合征的特征,并且由于世界的西方化而逐渐对发达国家和发展中国家造成沉重负担。由于代谢综合征的大多数特征似乎都源于中枢型肥胖,因此代谢综合征的潜在机制可以帮助我们了解肥胖-哮喘病的病理生物学。线粒体功能障碍是代谢综合征大多数危险因素的常见因素,例如中枢型肥胖,血脂异常,高血压,胰岛素抵抗和2型糖尿病,但线粒体参与肥胖-哮喘的发病机制似乎很重要,因为线粒体功能障碍最近已显示出与气道上皮损伤和哮喘发病机理有关。这篇综述讨论了目前对代谢综合征和哮喘与线粒体结构和功能改变有关的重叠特征的了解,旨在揭示肥胖哮喘的机制。

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