ArticleJCI insight2019
Oxidative hotspots on actin promote skeletal muscle weakness in rheumatoid arthritis.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06480643 (Effect of Exercise Type on Muscle Quality in Patients With OA, SARC and RA), which is not on this map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Effect of Exercise Type on Muscle Quality in Patients With OA, SARC and RA: an Explorative Study The Care for Muscle Study
Who cites it
18 citing papers in PubMed, 59 citations in OpenAlex.
- Trial
- Health-enhancing physical activity induce beneficial skeletal muscle mitochondrial adaptations in individuals with rheumatoid arthritis.Clinical rheumatology · 2025Article
- Identification biomarkers and therapeutic targets of disulfidptosis-related in rheumatoid arthritis via bioinformatics, molecular dynamics simulation, and experimental validation.Scientific reports · 2025Article
- Methodology Development for Investigating Pathophysiological [Biomedicines · 2025Article
- A new stress test for ryanodine receptors.The Journal of general physiology · 2024Article
- Stable oxidative posttranslational modifications alter the gating properties of RyR1.The Journal of general physiology · 2024Article
- Revisiting specific force loss in human permeabilized single skeletal muscle fibers obtained from older individuals.American journal of physiology. Cell physiology · 2023Article
- Platelets-related signature based diagnostic model in rheumatoid arthritis using WGCNA and machine learning.Frontiers in immunology · 2023Article
- Proteomics of fibrin amyloid microclots in long COVID/post-acute sequelae of COVID-19 (PASC) shows many entrapped pro-inflammatory molecules that may also contribute to a failed fibrinolytic system.Cardiovascular diabetology · 2022Article
- A pilot study on nitration/dysfunction of NK1 segment of myogenic stem cell activator HGF.Biochemistry and biophysics reports · 2022Article
- The potential role of ischaemia-reperfusion injury in chronic, relapsing diseases such as rheumatoid arthritis, Long COVID, and ME/CFS: evidence, mechanisms, and therapeutic implications.The Biochemical journal · 2022Review
- Removal of MuRF1 Increases Muscle Mass in Nemaline Myopathy Models, but Does Not Provide Functional Benefits.International journal of molecular sciences · 2022Article
- Unresolved intramuscular inflammation, not diminished skeletal muscle regenerative capacity, is at the root of rheumatoid cachexia: insights from a rat CIA model.Physiological reports · 2021Article
- Exercise protects against cardiac and skeletal muscle dysfunction in a mouse model of inflammatory arthritis.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- Fast skeletal muscle troponin activator CK-2066260 mitigates skeletal muscle weakness independently of the underlying cause.Journal of cachexia, sarcopenia and muscle · 2020Article
- Skeletal muscle redox signaling in rheumatoid arthritis.Clinical science (London, England : 1979) · 2020Review
- Article
- Intramuscular mechanisms of overtraining.Redox biology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 8 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal muscle weakness in patients suffering from rheumatoid arthritis (RA) adds to their impaired working abilities and reduced quality of life. However, little molecular insight is available on muscle weakness associated with RA. Oxidative stress has been implicated in the disease pathogenesis of RA. Here we show that oxidative post-translational modifications of the contractile machinery targeted to actin result in impaired actin polymerization and reduced force production. Using mass spectrometry, we identified the actin residues targeted by oxidative 3-nitrotyrosine (3-NT) or malondialdehyde adduct (MDA) modifications in weakened skeletal muscle from mice with arthritis and patients afflicted by RA. The residues were primarily located to three distinct regions positioned at matching surface areas of the skeletal muscle actin molecule from arthritis mice and RA patients. Moreover, molecular dynamic simulations revealed that these areas, here coined "hotspots", are important for the stability of the actin molecule and its capacity to generate filaments and interact with myosin. Together, these data demonstrate how oxidative modifications on actin promote muscle weakness in RA patients and provide novel leads for targeted therapeutic treatment to improve muscle function.
Indexed as
Identifiers
What OpenQuestion holds
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.