Clinica Medica, Dipartimento di Scienze Cliniche e Molecolari, Università Politecnica delle Marche, via Tronto 10/A, 60126 Torrette di Ancona, Italy; Postgraduate School of Allergy and Clinical Immunology, Università Politecnica delle Marche, via Tronto 10/A, 60126 Ancona, Italy.
PostGraduate School of Internal Medicine, Università Politecnica delle Marche, via Tronto 10/A, 60126 Ancona, Italy.
Autoimmun Rev. 2023 May;22(5):103308. doi: 10.1016/j.autrev.2023.103308. Epub 2023 Feb 21.
We investigated the relationship between oxidative stress and inflammatory myopathies. We searched in the current literature the role of mitochondria and respiratory chain defects as sources of oxidative stress and reactive oxygen species production that led to muscle weakness and fatigue. Different molecules and pathways contribute to redox milieu, reactive oxygen species generation, accumulation of misfolded and carbonylated proteins that lose their ability to fulfil cellular activities. Small peptides and physical techniques proved, in mice models, to reduce oxidative stress. We focused on inclusion body myositis, as a major expression of myopathy related to oxidative stress, where mitochondrial abnormalities are causative agents as well. We described the effect of physical exercise in inclusion body myositis that showed to increase strength and to reduce beta amyloid accumulation with subsequent improvement of the mitochondrial functions. We illustrated the influence of epigenetic control on the immune system by non-coding genetic material in the interaction between oxidative stress and inflammatory myopathies.
我们研究了氧化应激与炎性肌病之间的关系。我们在当前的文献中探讨了线粒体和呼吸链缺陷作为氧化应激和活性氧（ROS）产生的来源，这些应激和 ROS 导致肌肉无力和疲劳。不同的分子和途径有助于氧化还原环境、ROS 生成、错误折叠和羰基化蛋白质的积累，这些蛋白质丧失了完成细胞活动的能力。在小鼠模型中，小肽和物理技术已被证明可以减轻氧化应激。我们重点研究了包涵体肌炎，因为它是一种主要的与氧化应激相关的肌病表现，其中线粒体异常也是致病因素。我们描述了体育锻炼对包涵体肌炎的影响，发现它可以增强肌肉力量，减少β淀粉样蛋白的积累，从而改善线粒体功能。我们通过非编码遗传物质说明了氧化应激与炎性肌病之间的相互作用中，表观遗传控制对免疫系统的影响。
