ArticlePloS one2014
Metformin protects skeletal muscle from cardiotoxin induced degeneration.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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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
37 citing papers in PubMed, 57 citations in OpenAlex.
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- Metformin enhances external urethral sphincter integrity and restores continence via AMPK activation in a rat model of stress urinary incontinence.Animal models and experimental medicine · 2026Article
- Impact of obesity and an obesogenic environment on cardiotoxin-induced damage and recovery of human myotubes.Experimental physiology · 2026Article
- Obestatin Treatment Counteracts Muscle Wasting by Reactivation of Autophagy in Duchenne Muscular Dystrophy.MedComm · 2026Article
- Skeletal muscle-specific inducible AMPKα1/α2 knockout mice develop muscle weakness, glycogen depletion, and fibrosis that persists during disuse atrophy.American journal of physiology. Endocrinology and metabolism · 2024Article
- Severely Damaged Freeze-Injured Skeletal Muscle Reveals Functional Impairment, Inadequate Repair, and Opportunity for Human Stem Cell Application.Biomedicines · 2023Article
- Impact of metformin on statin-associated myopathy risks in dyslipidemia patients.Pharmacology research & perspectives · 2023Article
- Metformin Pre-Treatment as a Means of Mitigating Disuse-Induced Rat Soleus Muscle Wasting.Current issues in molecular biology · 2023Article
- Article
- Mechanisms and effects of metformin on skeletal muscle disorders.Frontiers in neurology · 2023Review
- Metformin Attenuates Slow-to-Fast Fiber Shift and Proteolysis Markers Increase in Rat Soleus after 7 Days of Rat Hindlimb Unloading.International journal of molecular sciences · 2022Article
- Upregulation of Wilms' Tumor 1 in epicardial cells increases cardiac fibrosis in dystrophic mice.Cell death and differentiation · 2022Article
- Protective Effect of Delta-Like 1 Homolog Against Muscular Atrophy in a Mouse Model.Endocrinology and metabolism (Seoul, Korea) · 2022Article
- Article
- Generation of Skeletal Muscle Organoids from Human Pluripotent Stem Cells to Model Myogenesis and Muscle Regeneration.International journal of molecular sciences · 2022Article
- Skeletal Muscle Uncoupling Proteins in Mice Models of Obesity.Metabolites · 2022Review
- Metformin and leucine increase satellite cells and collagen remodeling during disuse and recovery in aged muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- MetforminFrontiers in physiology · 2021Article
Corrections and comments
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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
The skeletal muscle tissue has a remarkable capacity to regenerate upon injury. Recent studies have suggested that this regenerative process is improved when AMPK is activated. In the muscle of young and old mice a low calorie diet, which activates AMPK, markedly enhances muscle regeneration. Remarkably, intraperitoneal injection of AICAR, an AMPK agonist, improves the structural integrity of muscles of dystrophin-deficient mdx mice. Building on these observations we asked whether metformin, a powerful anti-hyperglycemic drug, which indirectly activates AMPK, affects the response of skeletal muscle to damage. In our conditions, metformin treatment did not significantly influence muscle regeneration. On the other hand we observed that the muscles of metformin treated mice are more resilient to cardiotoxin injury displaying lesser muscle damage. Accordingly myotubes, originated in vitro from differentiated C2C12 myoblast cell line, become more resistant to cardiotoxin damage after pre-incubation with metformin. Our results indicate that metformin limits cardiotoxin damage by protecting myotubes from necrosis. Although the details of the molecular mechanisms underlying the protective effect remain to be elucidated, we report a correlation between the ability of metformin to promote resistance to damage and its capacity to counteract the increment of intracellular calcium levels induced by cardiotoxin treatment. Since increased cytoplasmic calcium concentrations characterize additional muscle pathological conditions, including dystrophies, metformin treatment could prove a valuable strategy to ameliorate the conditions of patients affected by dystrophies.
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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.