Association of Mitochondrial Dysfunction and Fatigue: A Review of the Literature.
Association of Mitochondrial Dysfunction and Fatigue: A Review of the Literature.
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DOI：
10.1016/j.bbacli.2014.04.001
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发表时间：
2014-06-01
期刊：
影响因子：
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通讯作者：
Saligan, Leorey N
中科院分区：
文献类型：
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作者：
Filler, Kristin;Lyon, Debra;Bennett, James;McCain, Nancy;Elswick, Ronald;Lukkahatai, Nada;Saligan, Leorey N
疲劳通常被患者描述为缺乏精力，精神或身体疲惫，耐力下降，在体力活动后恢复时间较长。疲劳的病因机制尚不清楚；然而，疲劳是线粒体疾病的标志症状，使线粒体功能障碍成为疲劳的可能生物学机制。因此，本文综述了线粒体功能障碍的标志物与疲劳的关系，并提出了可能的研究方向，以加强对线粒体功能障碍在疲劳中的作用的了解。使用PubMed、Scope us、Web of Science和Embase数据库进行彻底搜索，得到1220篇文章。在应用纳入和排除标准后，总共选择了25条符合资格标准的文章进行全面审查。线粒体结构、线粒体功能(线粒体酶和氧化/亚硝化应激)、线粒体能量代谢(ATP产生和脂肪酸代谢)、免疫反应和遗传学方面的功能障碍被研究为可能导致疲劳的因素。肉碱是研究最多的线粒体功能标志物。在所有研究肉碱的研究中都报告了功能障碍的水平；然而，功能障碍的特定类型的肉碱是不同的。遗传图谱是研究第二多的线粒体参数。提出了六条共同的途径：代谢、能量产生、蛋白质运输、线粒体形态、中枢神经系统功能障碍和病毒感染后。辅酶Q10是最常被研究的线粒体酶。低水平的辅酶Q10一直与疲劳有关。确定了进一步调查的潜在目标以及目前文献中的空白。疲劳症状背后的致病机制尚不清楚。本文就线粒体功能障碍与疲劳的关系作一综述。在线粒体功能障碍和疲劳之间观察到不一致的关联。
Fatigue is often described by patients as a lack of energy, mental or physical tiredness, diminished endurance, and prolonged recovery after physical activity. Etiologic mechanisms underlying fatigue are not well understood; however, fatigue is a hallmark symptom of mitochondrial disease, making mitochondrial dysfunction a putative biological mechanism for fatigue. Therefore, this review examined studies that investigated the association of markers of mitochondrial dysfunction with fatigue and proposes possible research directions to enhance understanding of the role of mitochondrial dysfunction in fatigue. A thorough search using PubMed, Scopus, Web of Science, and Embase databases returned 1220 articles. After the application of inclusion and exclusion criteria, a total of 25 articles meeting eligibility criteria were selected for full review. Dysfunctions in the mitochondrial structure, mitochondrial function (mitochondrial enzymes and oxidative/nitrosative stress), mitochondrial energy metabolism (ATP production and fatty acid metabolism), immune response, and genetics were investigated as potential contributors to fatigue. Carnitine was the most investigated mitochondrial function marker. Dysfunctional levels were reported in all the studies investigating carnitine; however, the specific type of carnitine that was dysfunctional varied. Genetic profiles were the second most studied mitochondrial parameter. Six common pathways were proposed: metabolism, energy production, protein transport, mitochondrial morphology, central nervous system dysfunction and post-viral infection. Coenzyme Q10 was the most commonly investigated mitochondrial enzyme. Low levels of Coenzyme Q10 were consistently associated with fatigue. Potential targets for further investigation were identified as well as gaps in the current literature. Etiologic mechanisms underlying the symptom of fatigue are not well understood. This review investigates the association of mitochondrial dysfunction with fatigue. Inconsistent associations observed between mitochondria dysfunction and fatigue.