ArticleRedox biology2019
A maladaptive ER stress response triggers dysfunction in highly active muscles of mice with SELENON loss.
Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 65 citations in OpenAlex.
- ER proteostasis meets mitochondrial function: contact sites as hubs of communication and therapeutic targets.The FEBS journal · 2026Review
- Selenoprotein N and SEPN1-Related Myopathies: Mechanisms, Models, and Therapeutic Perspectives.Biomolecules · 2026Review
- Lead (Pb) Induces Osteotoxicity Through the Activation of Mutually Reinforced ER Stress and ROS in MC3T3-E1 Cells.Biological trace element research · 2025Article
- Mitochondrial quality control as a therapeutic target in cardiovascular disease: Mechanistic insights and future directions.Journal of translational internal medicine · 2025Article
- Selenium and Skeletal Muscle Health in Sports Nutrition.Nutrients · 2025Review
- Zebrafish and cellular models of SELENON-Congenital myopathy exhibit novel embryonic and metabolic phenotypes.Skeletal muscle · 2025Article
- Small molecule-mediated inhibition of the oxidoreductase ERO1A restrains aggressive breast cancer by impairing VEGF and PD-L1 in the tumor microenvironment.Cell death & disease · 2025Article
- Mitochondria and myocardial ischemia/reperfusion injury: Effects of Chinese herbal medicine and the underlying mechanisms.Journal of pharmaceutical analysis · 2025Review
- Intracellular Membrane Contact Sites in Skeletal Muscle Cells.Membranes · 2025Review
- Endoplasmic reticulum oxidoreductin 1α as a potential therapeutic target in diseases: from oxidative protein folding to pathophysiological mechanisms.Frontiers in pharmacology · 2025Review
- Decoding interaction between mitochondria and endoplasmic reticulum in ischemic myocardial injury: targeting natural medicines.Frontiers in pharmacology · 2025Review
- A Novel MAO-B/SSAO Inhibitor Improves Multiple Aspects of Dystrophic Phenotype inAntioxidants (Basel, Switzerland) · 2024Article
- SEPN1-related myopathy depends on the oxidoreductase ERO1A and is druggable with the chemical chaperone TUDCA.Cell reports. Medicine · 2024Article
- ER stress and ERO1: Potential therapeutic targets for inherited myopathies.Cell reports. Medicine · 2024Article
- "Alphabet" Selenoproteins: Their Characteristics and Physiological Roles.International journal of molecular sciences · 2023Review
- Cerium Oxide Nanoparticles Protect Cortical Astrocytes from Oxygen-Glucose Deprivation through Activation of the CaInternational journal of molecular sciences · 2023Article
- Selenium and Selenoproteins in Health.Biomolecules · 2023Review
- Endoplasmic reticulum oxidoreductin 1-alpha deficiency and activation of protein translation synergistically impair breast tumour resilience.British journal of pharmacology · 2022Article
- Loss-of-rescue of Ryr1Scientific reports · 2022Article
- Mitochondrial ROS, ER Stress, and Nrf2 Crosstalk in the Regulation of Mitochondrial Apoptosis Induced by Arsenite.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Selenoprotein N (SELENON) is an endoplasmic reticulum (ER) protein whose loss of function leads to human SELENON-related myopathies. SelenoN knockout (KO) mouse limb muscles, however, are protected from the disease, and display no major alterations in muscle histology or contractile properties. Interestingly, we find that the highly active diaphragm muscle shows impaired force production, in line with the human phenotype. In addition, after repeated stimulation with a protocol which induces muscle fatigue, also hind limb muscles show altered relaxation times. Mechanistically, muscle SELENON loss alters activity-dependent calcium handling selectively impinging on the Ca
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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.