ArticleOxidative medicine and cellular longevity2022
Myostatin Deficiency Enhances Antioxidant Capacity of Bovine Muscle via the SMAD-AMPK-G6PD Pathway.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 14 citations in OpenAlex.
- Early Growth and Serum Metabolic Profiling of One-Month-Old MSTN-Knockout Xinjiang Brown Cattle via CRISPR/Cas12Mix.Animals : an open access journal from MDPI · 2026Article
- Exercise Impacts Liver Disease: Balancing Metabolic and Immune Homeostasis.International journal of biological sciences · 2026Review
- Circulating Biomarkers as a Window into the Relationship between Sarcopenia and Diabetes: Implications for Effective Management.Current diabetes reviews · 2026Review
- Integrated Transcriptomic and Metabolomic Analysis RevealsFoods (Basel, Switzerland) · 2025Article
- Molecular Mechanism of Aerobic Exercise Ameliorating Myocardial Mitochondrial Injury in Mice with Heart Failure.International journal of molecular sciences · 2025Article
- Myokines and Their Potential Protective Role Against Oxidative Stress in Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).Antioxidants (Basel, Switzerland) · 2024Review
- Roles of Myokines and Muscle-Derived Extracellular Vesicles in Musculoskeletal Deterioration under Disuse Conditions.Metabolites · 2024Review
- Energy Regulation in Inflammatory Sarcopenia by the Purinergic System.International journal of molecular sciences · 2023Review
- The Effect of MSTN Mutation on Bile Acid Metabolism and Lipid Metabolism in Cattle.Metabolites · 2023Article
- A Potential Negative Regulatory Function of Myostatin in the Growth of the Pacific Abalone,Biology · 2022Article
- Loss of Myostatin Alters Mitochondrial Oxidative Phosphorylation, TCA Cycle Activity, and ATP Production in Skeletal Muscle.International journal of molecular sciences · 2022Article
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11 authors at 1 institution in 1 country.
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Abstract
During exercise, the body's organs and skeletal muscles produce reactive oxygen species (ROS). Excessive ROS can destroy cellular lipids, sugars, proteins, and nucleotides and lead to cancer. The production of nicotinamide adenine dinucleotide phosphate (NADPH) by the pentose phosphate pathway (PPP) is an auxiliary process of the cellular antioxidant system that supplements the reducing power of glutathione (GSH) to eliminate ROS in the cell. Myostatin (MSTN) is mainly expressed in skeletal muscle and participates in the regulation of skeletal muscle growth and development. Loss of MSTN leads to muscular hypertrophy, and MSTN deficiency upregulates glycolysis. However, the effect of MSTN on the PPP has not been reported. This study investigated the effect of MSTN on muscle antioxidant capacity from a metabolic perspective. We found that reducing MSTN modulates AMP-activated protein kinase (AMPK), a key molecule in cellular energy metabolism that directly regulates glucose metabolism through phosphorylation. Downregulation of MSTN promotes tyrosine modification of glucose-6-phosphate-dehydrogenase (G6PD) by AMPK and is regulated by the Smad signaling pathway. The Smad2/3 complex acts as a transcription factor to inhibit the AMPK expression. These results suggest that reduced MSTN expression inhibits the Smad signaling pathway, promotes AMPK expression, enhances the activity of G6PD enzyme, and enhances the antioxidant capacity of nonenzymatic GSH.
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