Department of Physiology and Pharmacology, Molecular Muscle Physiology and Pathophysiology laboratory, Karolinska Institute, Stockholm, Sweden.
Clin Sci (Lond). 2020 Nov 13;134(21):2835-2850. doi: 10.1042/CS20190728.
Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by synovitis and the presence of serum autoantibodies. In addition, skeletal muscle weakness is a common comorbidity that contributes to inability to work and reduced quality of life. Loss in muscle mass cannot alone account for the muscle weakness induced by RA, but instead intramuscular dysfunction appears as a critical factor underlying the decreased force generating capacity for patients afflicted by arthritis. Oxidative stress and associated oxidative post-translational modifications have been shown to contribute to RA-induced muscle weakness in animal models of arthritis and patients with RA. However, it is still unclear how and which sources of reactive oxygen and nitrogen species (ROS/RNS) that are involved in the oxidative stress that drives the progression toward decreased muscle function in RA. Nevertheless, mitochondria, NADPH oxidases (NOX), nitric oxide synthases (NOS) and phospholipases (PLA) have all been associated with increased ROS/RNS production in RA-induced muscle weakness. In this review, we aim to cover potential ROS sources and underlying mechanisms of oxidative stress and loss of force production in RA. We also addressed the use of antioxidants and exercise as potential tools to counteract oxidative stress and skeletal muscle weakness.
类风湿关节炎（RA）是一种慢性炎症性疾病，其特征为滑膜炎和血清自身抗体的存在。此外，骨骼肌无力是一种常见的合并症，导致患者无法工作和生活质量下降。肌肉减少不能单独解释 RA 引起的肌肉无力，而肌肉内功能障碍似乎是关节炎患者肌力下降的关键因素。氧化应激和相关的氧化翻译后修饰已被证明可导致关节炎动物模型和 RA 患者的肌肉无力。然而，目前尚不清楚哪种来源的活性氧和活性氮物质（ROS/RNS）参与了导致 RA 肌肉功能下降的氧化应激。尽管如此，线粒体、NADPH 氧化酶（NOX）、一氧化氮合酶（NOS）和磷脂酶（PLA）都与 RA 诱导的肌肉无力时 ROS/RNS 的产生增加有关。在这篇综述中，我们旨在涵盖 RA 中潜在的 ROS 来源和氧化应激及肌力丧失的潜在机制。我们还讨论了抗氧化剂和运动作为对抗氧化应激和骨骼肌无力的潜在工具的使用。
