Skeletal muscle redox signaling in rheumatoid arthritis.
Skeletal muscle redox signaling in rheumatoid arthritis.
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DOI：
10.1042/cs20190728
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发表时间：
2020-11-13
期刊：
影响因子：
--
通讯作者：
Lanner JT
中科院分区：
文献类型：
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作者：
Steinz MM;Santos-Alves E;Lanner JT
类风湿性关节炎（RA）是一种以滑膜炎和血清自身抗体为特征的慢性炎症性疾病。此外，骨骼肌无力是一种常见的合并症，导致无法工作和生活质量下降。肌肉质量的损失不能单独解释由RA引起的肌肉无力，而是肌内功能障碍似乎是关节炎患者产生力能力降低的关键因素。在关节炎动物模型和RA患者中，氧化应激和相关的氧化翻译后修饰已被证明有助于RA诱导的肌无力。然而，目前尚不清楚活性氧和氮物质（ROS/RNS）如何以及哪些来源参与氧化应激，从而导致RA肌肉功能下降。然而，线粒体、NADPH氧化酶（NOX）、一氧化氮合酶（NOS）和磷脂酶（PLA）都与RA诱导的肌无力中ROS/RNS产生增加相关。在这篇综述中，我们的目的是涵盖潜在的活性氧来源和潜在的机制，氧化应激和损失的力量生产在RA。我们还讨论了使用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。
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.