Arginine and nitric oxide pathways in obesity-associated asthma.
Arginine and nitric oxide pathways in obesity-associated asthma.
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DOI：
10.1155/2013/714595
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发表时间：
2013
期刊：
影响因子：
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通讯作者：
Holguin F
中科院分区：
文献类型：
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作者：
Holguin F
肥胖是一种共病，对哮喘的严重程度和控制机制产生不利影响，但机制尚不完全清楚。这篇综述将讨论支持一氧化氮(NO)作为肥胖和迟发性哮喘之间潜在机制联系的证据(>；12年)。多项研究表明，体重指数(BMI)的增加和NO呼出量的减少之间存在负相关。更新的证据表明，这种矛盾关系的一个潜在解释与一氧化氮合酶解偶联有关，一氧化氮合酶解偶联是由于一氧化氮合酶底物L精氨酸与其内源性抑制物不对称二甲基精氨酸之间的失衡所致。这篇综述将提出一个理论框架，以理解这一途径的相关性，以及它在早发和晚发肥胖哮喘患者之间的差异。最后，本文将讨论基于这些范例的潜在新的治疗方法，以改善患有哮喘的肥胖患者的呼吸健康。
Obesity is a comorbidity that adversely affects asthma severity and control by mechanisms that are not fully understood. This review will discuss evidence supporting a role for nitric oxide (NO) as a potential mechanistic link between obesity and late-onset asthma (>12 years). Several studies have shown that there is an inverse association between increasing body mass index (BMI) and reduced exhaled NO. Newer evidence suggests that a potential explanation for this paradoxical relationship is related to nitric oxide synthase (NOS) uncoupling, which occurs due to an imbalance between L-arginine (NOS substrate) and its endogenous inhibitor, asymmetric di-methyl arginine (ADMA). The review will propose a theoretical framework to understand the relevance of this pathway and how it may differ between early and late-onset obese asthmatics. Finally, the paper will discuss potential new therapeutic approaches, based on these paradigms, for improving the respiratory health of obese subjects with asthma.