ReviewClinical science (London, England : 1979)2020
Skeletal muscle redox signaling in rheumatoid arthritis.
Review in Clinical science (London, England : 1979), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 34 citations in OpenAlex.
- The Roles of Complementary Structured Exercise and Physical Therapy in The Aging and Older Adult IBD Patient Care Team.Current treatment options in gastroenterology · 2026Article
- Nanometer preparation of natural bioactive compounds for treatment of rheumatoid arthritis.Journal of pharmaceutical analysis · 2025Review
- Health-enhancing physical activity induce beneficial skeletal muscle mitochondrial adaptations in individuals with rheumatoid arthritis.Clinical rheumatology · 2025Article
- Effects of Low and High Maternal Protein Intake on Fetal Skeletal Muscle miRNAome in Sheep.Animals : an open access journal from MDPI · 2024Article
- Activatable fluorescent probes for imaging and diagnosis of rheumatoid arthritis.Military Medical Research · 2023Review
- Mechanistic and therapeutic links between rheumatoid arthritis and diabetes mellitus.Clinical and experimental medicine · 2023Review
- Adding High-Intensity Interval Training to Classical Resistance Training Does Not Impede the Recovery from Inactivity-Induced Leg Muscle Weakness.Antioxidants (Basel, Switzerland) · 2022Article
- Prevalence of sarcopenia in patients with rheumatoid arthritis using the revised EWGSOP2 and the FNIH definition.RMD open · 2022Observational
- Microbiota-assisted therapy for systemic inflammatory arthritis: advances and mechanistic insights.Cellular and molecular life sciences : CMLS · 2022Review
- Lysyl oxidase-like 2 inhibitor rescues D-galactose-induced skeletal muscle fibrosis.Aging cell · 2022Article
- The Role of Oxidative Stress in Skeletal Muscle Myogenesis and Muscle Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Mitochondrial Function and Reactive Oxygen/Nitrogen Species in Skeletal Muscle.Frontiers in cell and developmental biology · 2022Review
- COVID-19 and Rheumatoid Arthritis Crosstalk: Emerging Association, Therapeutic Options and Challenges.Cells · 2021Review
- Claudin-5 Affects Endothelial Autophagy in Response to Early Hypoxia.Frontiers in physiology · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.