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An Updated Overview of Metabolomic Profile Changes in Chronic Obstructive Pulmonary Disease

机译:慢性阻塞性肺疾病的代谢组学谱变化的最新概述。

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摘要

Chronic obstructive pulmonary disease (COPD), a common and heterogeneous respiratory disease, is characterized by persistent and incompletely reversible airflow limitation. Metabolomics is applied to analyze the difference of metabolic profile based on the low-molecular-weight metabolites (<1 kDa). Emerging metabolomic analysis may provide insights into the pathogenesis and diagnosis of COPD. This review aims to summarize the alteration of metabolites in blood/serum/plasma, urine, exhaled breath condensate, lung tissue samples, etc. from COPD individuals, thereby uncovering the potential pathogenesis of COPD according to the perturbed metabolic pathways. Metabolomic researches have indicated that the dysfunctions of amino acid metabolism, lipid metabolism, energy production pathways, and the imbalance of oxidations and antioxidations might lead to local and systematic inflammation by activating the Nuclear factor kappa-light-chain-enhancer of activated B cells signaling pathway and releasing inflammatory cytokines, like interleutin-6 (IL-6), tumor necrosis factor-α, and IL-8. In addition, they might cause protein malnutrition and oxidative stress and contribute to the development and exacerbation of COPD.
机译:慢性阻塞性肺疾病(COPD)是一种常见的异质性呼吸系统疾病,其特征是持续的和不完全可逆的气流受限。代谢组学被用于分析基于低分子量代谢物(<1 kDa)的代谢谱的差异。新兴的代谢组学分析可为COPD的发病机理和诊断提供见识。这篇综述旨在总结COPD个体血液/血清/血浆,尿液,呼出气冷凝物,肺组织样本等中代谢物的变化,从而根据扰动的代谢途径揭示COPD的潜在发病机理。代谢组学研究表明,氨基酸代谢功能异常,脂质代谢,能量产生途径以及氧化和抗氧化失衡可能通过激活活化的B细胞信号转导核因子κ轻链增强剂而导致局部和系统性炎症。途径并释放炎性细胞因子,例如白介素6(IL-6),肿瘤坏死因子-α和IL-8。另外,它们可能引起蛋白质营养不良和氧化应激,并导致COPD的发展和恶化。

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