线粒体失衡是研究纤维肌痛的新途径。

IF 1.7 Q3 RHEUMATOLOGY
Open Access Rheumatology-Research and Reviews Pub Date : 2020-08-24 eCollection Date: 2020-01-01 DOI:10.2147/OARRR.S257470
Antonio Martínez-Lara, Ana María Moreno-Fernández, Maripaz Jiménez-Guerrero, Claudia Díaz-López, Manuel De-Miguel, David Cotán, José Antonio Sánchez-Alcázar
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引用次数: 4

摘要

背景:纤维肌痛(FM)是一种常见的慢性疼痛疾病,其发病机制尚不明确。氧化应激标志物和生物能量平衡受损被认为是该疾病发病机制中的相关事件。因此,本研究的目的是分析FM患者线粒体失衡的潜在生物标志物以及辅酶Q10 (CoQ10)作为可能的治疗方法。方法:采用纤维肌痛影响问卷(FIQ)对患者的症状进行记录。对33例确诊为FM的患者和30例健康对照者进行了抽血和血清分离检测线粒体失衡。采用Western blot和HPLC技术对不同参数进行研究。最后,对机器学习进行生物信息学分析,以预测结果之间可能存在的关联。结果:CoQ10参数没有证据表明是疾病的良好标志物,因为对照组和患者组之间的值没有显着差异(学生t检验,CI 95%)。因此,研究的重点转向了线粒体质量与自噬水平的比值。生物信息学分析显示这一比例与患者的症状之间可能存在关联。最后,辅酶Q10作为一种潜在的治疗疾病的效果在患者体内是不同的,其疗效可能与初始线粒体状态有关。然而,由于样本量的限制,没有统计学意义。结论:我们的研究支持了线粒体稳态失衡参与FM发病机制的假设。然而,氧化应激的增加是线粒体失衡的结果还是这种疾病的原因仍然是一个悬而未决的问题。这种不平衡的测量可以作为FM患者诊断和随访的初步生物标志物,甚至可以用于评估不同抗氧化剂治疗的效果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Mitochondrial Imbalance as a New Approach to the Study of Fibromyalgia.

Mitochondrial Imbalance as a New Approach to the Study of Fibromyalgia.

Mitochondrial Imbalance as a New Approach to the Study of Fibromyalgia.

Mitochondrial Imbalance as a New Approach to the Study of Fibromyalgia.

Background: Fibromyalgia (FM) is a common chronic pain disease, whose pathogenic mechanism still remains elusive. Oxidative stress markers and impaired bioenergetics homeostasis have been proposed as relevant events in the pathogenesis of the disease. Hence, the aim of the study is to analyse the potential biomarkers of mitochondrial imbalance in FM patients along with coenzyme Q10 (CoQ10) as a possible treatment.

Methods: The symptomatology of patients was recorded with an adaption of the Fibromyalgia Impact Questionnaire (FIQ). Mitochondrial imbalance was tested from blood extraction and serum isolation in 33 patients diagnosed with FM and 30 healthy controls. Western blot and HPLC techniques were performed to study the different parameters. Finally, bioinformatic analysis of machine learning was performed to predict possible associations of results.

Results: CoQ10 parameter did not show evidence to be a good marker of the disease, as the values are not significantly different between control and patient groups (Student's t-test, CI 95%). For this reason, the focus of the study changed into the ratio between mitochondrial mass and autophagy levels. The bioinformatics analysis showed a possible association between this ratio and patients' symptomatology. Finally, the effects of coenzyme Q10 as a potential treatment for the disease were different within patients, and its efficacy may be related to the initial mitochondrial status. However, there is no statistical significance due to limitations within the sample size.

Conclusion: Our study supports the hypothesis that an imbalance in mitochondrial homeostasis is involved in the FM pathogenesis. However, whether the increase in oxidative stress is the result of mitochondrial imbalance or the cause of this disease remains an open question. The measurement of this imbalance might be used as a preliminary biomarker for the diagnosis and follow-up of patients with FM, and even for the evaluation of the effects of the different antioxidants therapies.

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来源期刊
CiteScore
3.80
自引率
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