ArticleOxidative medicine and cellular longevity2016
Creatine Prevents the Structural and Functional Damage to Mitochondria in Myogenic, Oxidatively Stressed C2C12 Cells and Restores Their Differentiation Capacity.
Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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30 citing papers in PubMed, 43 citations in OpenAlex.
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- Revision of Energy Metabolism Adaptations in High-Level Athletes: From Physical Performance Enhancement to Potential Therapeutic Targets in Mental Disorders.Current issues in molecular biology · 2026Review
- Creatine increases muscle fiber size in embryonic chick muscle cells and age-dependent swimming performance in zebrafish.Scientific reports · 2026Article
- Energy metabolism dysregulation in idiopathic inflammatory myopathies: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- The Post-COVID syndrome caused by excessive inflammation: pathogenesis, potential targets and therapeutic agents.Frontiers in pharmacology · 2026Review
- Creatine as a mitochondrial theranostic in predictive, preventive, and personalized medicine.The EPMA journal · 2025Review
- Effects of SLC6A8 mutation-induced creatine deficiency on cellular function in fibroblasts.Scientific reports · 2025Article
- Low-molecular-weight whey protein hydrolysate and ginseng berry extract enhance muscle strength and physical performance in Korean older adults: a randomized controlled trial.Nutrition research and practice · 2025Article
- Creatine mitigates neurogenesis impairment caused by defective DcpS decapping.Scientific reports · 2025Article
- Eight weeks of creatine monohydrate supplementation is associated with increased muscle strength and size in Alzheimer's disease: data from a single-arm pilot study.Frontiers in nutrition · 2025Article
- Mitochondrial stress response and myogenic differentiation.Frontiers in cell and developmental biology · 2024Review
- Proteomic and metabolomic analysis of GH deficiency-induced NAFLD in hypopituitarism: insights into oxidative stress.Frontiers in endocrinology · 2024Article
- Analysis revealed the molecular mechanism of oxidative stress-autophagy-induced liver injury caused by high alkalinity: integrated whole hepatic transcriptome and metabolome.Frontiers in immunology · 2024Article
- Efficacy of creatine nitrate supplementation on redox status and mitochondrial function inAnimal biotechnology · 2023Article
- Creatine Supplementation Potentiates Exercise Protective Effects against Doxorubicin-Induced Hepatotoxicity in Mice.Antioxidants (Basel, Switzerland) · 2023Article
- Advances in nutritional supplementation for sarcopenia management.Frontiers in nutrition · 2023Review
- In Vitro Modeling of Diabetes Impact on Vascular Endothelium: Are Essentials Engaged to Tune Metabolism?Biomedicines · 2022Review
- Mitochondrial Inorganic Polyphosphate (polyP) Is a Potent Regulator of Mammalian Bioenergetics in SH-SY5Y Cells: A Proteomics and Metabolomics Study.Frontiers in cell and developmental biology · 2022Article
- The Effects of In Utero Fetal Hypoxia and Creatine Treatment on Mitochondrial Function in the Late Gestation Fetal Sheep Brain.Oxidative medicine and cellular longevity · 2022Article
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Creatine (Cr) is a nutritional supplement promoting a number of health benefits. Indeed Cr has been shown to be beneficial in disease-induced muscle atrophy, improve rehabilitation, and afford mild antioxidant activity. The beneficial effects are likely to derive from pleiotropic interactions. In accord with this notion, we previously demonstrated that multiple pleiotropic effects, including preservation of mitochondrial damage, account for the capacity of Cr to prevent the differentiation arrest caused by oxidative stress in C2C12 myoblasts. Given the importance of mitochondria in supporting the myogenic process, here we further explored the protective effects of Cr on the structure, function, and networking of these organelles in C2C12 cells differentiating under oxidative stressing conditions; the effects on the energy sensor AMPK, on PGC-1α, which is involved in mitochondrial biogenesis and its downstream effector Tfam were also investigated. Our results indicate that damage to mitochondria is crucial in the differentiation imbalance caused by oxidative stress and that the Cr-prevention of these injuries is invariably associated with the recovery of the normal myogenic capacity. We also found that Cr activates AMPK and induces an upregulation of PGC-1α expression, two events which are likely to contribute to the protection of mitochondrial quality and function.
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