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人体是一个能量混合体?慢性病治疗的新视角?

The human body as an energetic hybrid? New perspectives for chronic disease treatment?

作者信息

Gajewski Michał, Rzodkiewicz Przemysław, Maśliński Sławomir

机构信息

Department of Biochemistry and Molecular Biology, National Institute of Geriatrics, Rheumatology and Rehabilitation, Warsaw, Poland.

Department of Gerontology and Public Health, National Institute of Geriatrics, Rheumatology and Rehabilitation, Warsaw, Poland.

出版信息

Reumatologia. 2017;55(2):94-99. doi: 10.5114/reum.2017.67605. Epub 2017 Apr 28.

DOI:10.5114/reum.2017.67605
PMID:28539682
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5442301/
Abstract

Inflammatory response is accompanied by changes in cellular energy metabolism. Proinflammatory mediators like plasma C-reactive protein, IL-6, plasminogen activator inhibitor-1, TNF-α or monocyte chemoattractant protein-1 released in the site of inflammation activates immune cells and increase energy consumption. Increased demand for energy creates local hypoxia and lead in consequence to mitochondrial dysfunction. Metabolism of cells is switched to anaerobic glycolysis. Mitochondria continuously generate free radicals that what result in imbalance that causes oxidative stress, which results in oxidative damage. Chronic energy imbalance promotes oxidative stress, aging, and neurodegeneration and is associated with numerous disorders like Alzheimer's disease, multiple sclerosis, Parkinson's disease or Huntington's disease. It is also believed that oxidative stress and the formation of free radicals play an important role in the pathogenesis of rheumatoid diseases including especially rheumatoid arthritis. Pharmacological control of energy metabolism disturbances may be valuable therapeutic strategy of treatment of this disorders. In recent review we sum up knowledge related to energy disturbances and discuss phenomena such as zombies or hibernation which may indicate the potential targets for regulation of energy metabolism.

摘要

炎症反应伴随着细胞能量代谢的变化。炎症部位释放的促炎介质,如血浆C反应蛋白、白细胞介素-6、纤溶酶原激活物抑制剂-1、肿瘤坏死因子-α或单核细胞趋化蛋白-1,会激活免疫细胞并增加能量消耗。对能量的需求增加会导致局部缺氧,进而导致线粒体功能障碍。细胞代谢转向无氧糖酵解。线粒体持续产生自由基,这会导致失衡,进而引起氧化应激,导致氧化损伤。慢性能量失衡会促进氧化应激、衰老和神经退行性变,并与许多疾病相关,如阿尔茨海默病、多发性硬化症、帕金森病或亨廷顿病。人们还认为,氧化应激和自由基的形成在包括类风湿性关节炎在内的类风湿疾病的发病机制中起重要作用。药物控制能量代谢紊乱可能是治疗这些疾病的有价值的治疗策略。在最近的综述中,我们总结了与能量紊乱相关的知识,并讨论了诸如僵尸或冬眠等现象,这些现象可能指明了调节能量代谢的潜在靶点。