ArticleOncotarget2016
Selenoprotein W redox-regulated Ca2+ channels correlate with selenium deficiency-induced muscles Ca2+ leak.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 63 citations in OpenAlex.
- Low Selenium Diet Inhibited CaMKII Activation via miR-365-3p/SelT Signaling Axis, Resulting in Myoblast Differentiation Disorders and Skeletal Muscle Damage in Broilers.Biological trace element research · 2025Article
- Selenium and Skeletal Muscle Health in Sports Nutrition.Nutrients · 2025Review
- Impaired Upper Airway Muscle Function with Excessive or Deficient Dietary Intake of Selenium in Rats.Antioxidants (Basel, Switzerland) · 2024Article
- Research progress on the biological regulatory mechanisms of selenium on skeletal muscle in broilers.Poultry science · 2024Review
- Comparison of Sodium Selenite and Selenium-Enriched Spirulina Supplementation Effects After Selenium Deficiency on Growth, Tissue Selenium Concentrations, Antioxidant Activities, and Selenoprotein Expression in Rats.Biological trace element research · 2024Article
- The antioxidant barrier, oxidative/nitrosative stress, and protein glycation in allergy: from basic research to clinical practice.Frontiers in immunology · 2024Review
- Dietary selenium intake and sarcopenia in American adults.Frontiers in nutrition · 2024Article
- Aberrant Gene Expression of Selenoproteins in Chicken Spleen Lymphocytes Induced by Mercuric Chloride.Biological trace element research · 2022Article
- Comparative Proteomic Analysis Reveals the Effect of Selenoprotein W Deficiency on Oligodendrogenesis in Fear Memory.Antioxidants (Basel, Switzerland) · 2022Article
- Beyond antioxidants: Selenium and skeletal muscle mitochondria.Frontiers in veterinary science · 2022Review
- Immunomodulatory effects of selenium-enriched peptides from soybean in cyclophosphamide-induced immunosuppressed mice.Food science & nutrition · 2021Article
- The Impact of Selenium Deficiency on Cardiovascular Function.International journal of molecular sciences · 2021Review
- Roles of Selenoproteins in Brain Function and the Potential Mechanism of Selenium in Alzheimer's Disease.Frontiers in neuroscience · 2021Review
- Selenium at theFrontiers in neuroscience · 2021Review
- Avian Stress-Related Transcriptome and Selenotranscriptome: Role during Exposure to Heavy Metals and Heat Stress.Antioxidants (Basel, Switzerland) · 2019Review
- Selenium-Dependent Antioxidant Enzymes: Actions and Properties of Selenoproteins.Antioxidants (Basel, Switzerland) · 2018Review
- Selenium suppresses inflammation by inducing microRNA-146a inOncotarget · 2017Article
- Selenium against lead-induced apoptosis in chicken nervous tissues via mitochondrial pathway.Oncotarget · 2017Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Selenium (Se) deficiency induces Ca2+ leak and calcification in mammal skeletal muscles; however, the exact mechanism is still unclear. In the present study, both Se-deficient chicken muscle models and selenoprotein W (SelW) gene knockdown myoblast and embryo models were used to study the mechanism. The results showed that Se deficiency-induced typical muscular injuries accompanied with Ca2+ leak and oxidative stress (P < 0.05) injured the ultrastructure of the sarcoplasmic reticulum (SR) and mitochondria; decreased the levels of the Ca2+ channels, SERCA, SLC8A, CACNA1S, ORAI1, STIM1, TRPC1, and TRPC3 (P < 0.05); and increased the levels of Ca2+ channel PMCA (P < 0.05). Similarly, SelW knockdown also induced Ca2+ leak from the SR and cytoplasm; increased mitochondrial Ca2+ levels and oxidative stress; injured SR and mitochondrial ultrastructure; decreased levels of SLC8A, CACNA1S, ORA1, TRPC1, and TRPC3; and caused abnormal activities of Ca2+ channels in response to inhibitors in myoblasts and chicken embryos. Thus, both Se deficiency and SelW knockdown induced Ca2+ leak, oxidative stress, and Ca2+ channel reduction. In addition, Ca2+ levels and the expression of the Ca2+ channels, RyR1, SERCA, CACNA1S, TRPC1, and TRPC3 were recovered to normal levels by N-acetyl-L-cysteine (NAC) treatment compared with SelW knockdown cells. Thus, with regard to the decreased Ca2+ channels, SelW knockdown closely correlated Se deficiency with Ca2+ leak in muscles. The redox regulation role of SelW is crucial in Se deficiency-induced Ca2+ leak in muscles.
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