ReviewJournal of muscle research and cell motility2015
Emerging importance of oxidative stress in regulating striated muscle elasticity.
Review in Journal of muscle research and cell motility, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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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.
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Who cites it
50 citing papers in PubMed, 72 citations in OpenAlex.
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- Evidence for a role of adverse sarcomere signaling in atrial fibrillation induction.Journal of molecular and cellular cardiology plus · 2026Review
- Ferroportin inhibition attenuates pulmonary hypertension in hypoxic sickle cell disease mice.Blood advances · 2026Article
- Prognostic value of skeletal muscle viscoelasticity in older patients with heart failure: the VISMARC-HF study design.BMC geriatrics · 2026Observational
- The treatment of selected traditional Chinese medicine prescriptions and their metabolites for heart failure with preserved ejection fraction from basic science discovery to the clinic.Frontiers in pharmacology · 2026Review
- Potential Causal Relationships Between Circulating Micronutrient Levels and Multiple Neuroimmune Diseases: A Genetic Association Analysis.Brain and behavior · 2025Article
- Mechanically weak and highly dynamic state of mechanosensitive titin Ig domains induced by proline isomerization.Nature communications · 2025Article
- Reactive oxygen species in the pathogenesis of sarcopenia.Free radical biology & medicine · 2025Review
- Fatiguing exercise reduces cellular passive Young's modulus in human vastus lateralis muscle.Experimental physiology · 2024Article
- Saliva as a Diagnostic Tool for Early Detection of Exercise-Induced Oxidative Damage in Female Athletes.Biomedicines · 2024Article
- Episodic Binge-like Ethanol Reduces Skeletal Muscle Strength Associated with Atrophy, Fibrosis, and Inflammation in Young Rats.International journal of molecular sciences · 2023Article
- Urinary titin is not an early biomarker of skeletal muscle atrophy induced by muscle denervation in mice.PloS one · 2023Article
- Titin (TTN): from molecule to modifications, mechanics, and medical significance.Cardiovascular research · 2022Review
- Article
- Measurement of Lipid Peroxidation Products and Creatine Kinase in Blood Plasma and Saliva of Athletes at Rest and following Exercise.Journal of clinical medicine · 2022Article
- Protein Quality Control at the Sarcomere: Titin Protection and Turnover and Implications for Disease Development.Frontiers in physiology · 2022Review
- The titin N2B and N2A regions: biomechanical and metabolic signaling hubs in cross-striated muscles.Biophysical reviews · 2021Review
- Identification and Quantification of Glutathionylated Cysteines under Ischemic Stress.Journal of proteome research · 2021Article
- Diazoxide and Exercise Enhance Muscle Contraction during Obesity by Decreasing ROS Levels, Lipid Peroxidation, and Improving Glutathione Redox Status.Antioxidants (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The contractile function of striated muscle cells is altered by oxidative/nitrosative stress, which can be observed under physiological conditions but also in diseases like heart failure or muscular dystrophy. Oxidative stress causes oxidative modifications of myofilament proteins and can impair myocyte contractility. Recent evidence also suggests an important effect of oxidative stress on muscle elasticity and passive stiffness via modifications of the giant protein titin. In this review we provide a short overview of known oxidative modifications in thin and thick filament proteins and then discuss in more detail those oxidative stress-related modifications altering titin stiffness directly or indirectly. Direct modifications of titin include reversible disulfide bonding within the cardiac-specific N2-Bus domain, which increases titin stiffness, and reversible S-glutathionylation of cryptic cysteines in immunoglobulin-like domains, which only takes place after the domains have unfolded and which reduces titin stiffness in cardiac and skeletal muscle. Indirect effects of oxidative stress on titin can occur via reversible modifications of protein kinase signalling pathways (especially the NO-cGMP-PKG axis), which alter the phosphorylation level of certain disordered titin domains and thereby modulate titin stiffness. Oxidative stress also activates proteases such as matrix-metalloproteinase-2 and (indirectly via increasing the intracellular calcium level) calpain-1, both of which cleave titin to irreversibly reduce titin-based stiffness. Although some of these mechanisms require confirmation in the in vivo setting, there is evidence that oxidative stress-related modifications of titin are relevant in the context of biomarker design and represent potential targets for therapeutic intervention in some forms of muscle and heart disease.
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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.