ArticleThe FEBS journal2014
(-)-Epicatechin improves mitochondrial-related protein levels and ameliorates oxidative stress in dystrophic δ-sarcoglycan null mouse striated muscle.
Article in The FEBS journal, 2014. 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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Who cites it
30 citing papers in PubMed, 58 citations in OpenAlex.
- Epigenetic modulation of the gut-muscle axis in pompe disease: Microbiota fingerprints to cellular and molecular pathomechanisms.Molecular metabolism · 2026Review
- Effect of (-)-Epicatechin on Mitochondrial Homeostasis in Skeletal Muscle of Female Obese Rats.Molecules (Basel, Switzerland) · 2026Article
- (-)-Epicatechin accelerates muscle repair and promotes hypertrophy in type 2 fibers of BaCl2-damaged gastrocnemius in CD1 mice.Journal of molecular histology · 2026Article
- Interaction of Programmed Obesity and Postnatal High Fat Diet but Not (-)-Epicatechin Treatment Modifies Muscle Atrophy Proteins Levels in Male Wistar Rats.Cell biochemistry and biophysics · 2025Article
- Effects of Epicatechin on the Expression of MyomiRs-31, -133, -136, -206, -296, and -486 in the Skeletal Muscle of the Offspring of Obese Mothers.Cell biochemistry and biophysics · 2025Article
- Decoding Neuromuscular Disorders: The Complex Role of Genetic and Epigenetic Regulators.Genes · 2025Review
- Model organisms for investigating the functional involvement of NRF2 in non-communicable diseases.Redox biology · 2025Review
- Review
- Muscular Dystrophies.Advances in experimental medicine and biology · 2025Review
- Epicatechin-mediated modulation of the Nrf2/HO-1 pathway alleviates senile cerebral ischemic/reperfusion injury.Food science & nutrition · 2024Article
- Pharmacological Treatments and Therapeutic Targets in Muscle Dystrophies Generated by Alterations in Dystrophin-Associated Proteins.Medicina (Kaunas, Lithuania) · 2024Review
- Mitochondria and Reactive Oxygen Species: The Therapeutic Balance of Powers for Duchenne Muscular Dystrophy.Cells · 2024Review
- (-)-Epicatechin Ameliorates Cardiac Fibrosis in a Female Rat Model of Pre-Heart Failure with Preserved Ejection Fraction.Journal of medicinal food · 2022Article
- (-)-Epicatechin Reverses Glucose Intolerance in Rats Housed at Thermoneutrality.Planta medica · 2022Article
- (-)-Epicatechin Improves Vasoreactivity and Mitochondrial Respiration in Thermoneutral-Housed Wistar Rat Vasculature.Nutrients · 2022Article
- (-)-Epicatechin Alters Reactive Oxygen and Nitrogen Species Production Independent of Mitochondrial Respiration in Human Vascular Endothelial Cells.Oxidative medicine and cellular longevity · 2022Article
- Anticancer potential of (-)-epicatechin in a triple-negative mammary gland model.The Journal of pharmacy and pharmacology · 2021Article
- Dietary Cocoa Flavanols Enhance Mitochondrial Function in Skeletal Muscle and Modify Whole-Body Metabolism in Healthy Mice.Nutrients · 2021Article
- (-)-Epicatechin-Enriched Extract fromAntioxidants (Basel, Switzerland) · 2021Article
- Dietary cocoa ameliorates non-alcoholic fatty liver disease and increases markers of antioxidant response and mitochondrial biogenesis in high fat-fed mice.The Journal of nutritional biochemistry · 2021Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
Muscular dystrophies (MDs) are a group of heterogeneous genetic disorders characterized by progressive striated muscle wasting and degeneration. Although the genetic basis for many of these disorders has been identified, the exact mechanism of disease pathogenesis remains unclear. The presence of oxidative stress (OS) is known to contribute to the pathophysiology and severity of the MD. Mitochondrial dysfunction is observed in MD, and probably represents an important determinant of increased OS. Experimental antioxidant therapies have been implemented with the aim of protecting against disease progression, but results from clinical trials have been disappointing. In this study, we explored the capacity of the cacao flavonoid (-)-epicatechin (Epi) to mitigate OS by acting as a positive regulator of mitochondrial structure/function endpoints and redox balance control systems in skeletal and cardiac muscles of dystrophic, δ-sarcoglycan (δ-SG) null mice. Wild-type or δ-SG null 2.5-month-old male mice were treated via oral gavage with either water (controls) or Epi (1 mg·kg(-1) , twice daily) for 2 weeks. The results showed significant normalization of total protein carbonylation, recovery of the glutathione/oxidized glutathione ratio and enhanced superoxide dismutase 2, catalase and citrate synthase activities with Epi treatment. These effects were accompanied by increases in the protein levels of thioredoxin, glutathione peroxidase, superoxide dismutase 2, catalase, and mitochondrial endpoints. Furthermore, we found decreases in heart and skeletal muscle fibrosis, accompanied by an improvement in skeletal muscle function, with treatment. These results warrant further investigation of Epi as a potential therapeutic agent to mitigate MD-associated muscle degeneration.
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Registered trials
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