ArticleExperimental physiology2011
Increased catalase expression improves muscle function in mdx mice.
Article in Experimental physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- The burden, epidemiology, costs and treatment for Duchenne muscular dystrophy: an evidence review.Orphanet journal of rare diseases · 2017Pooled it
- Dystrophin Deficiency Creates a Pro-Ferroptotic Environment in Diaphragm of mdx Mice That Is Modified by Diet and Glucocorticoid Treatment.Biomolecules · 2026Article
- Long-term imoxin treatment does not attenuate disease severity in dystrophic diaphragm of male mice.Physiological reports · 2026Article
- A high-fat, high-sucrose diet exacerbates muscle and metabolic pathology and undermines glucocorticoid efficacy in dystrophin-deficient mice.The Journal of physiology · 2026Article
- Trilobatin contributes to the improvement of myopathy in a mouse model of Duchenne muscular dystrophy.International journal of experimental pathology · 2024Article
- Mitochondria and Reactive Oxygen Species: The Therapeutic Balance of Powers for Duchenne Muscular Dystrophy.Cells · 2024Review
- Comparative Proteomics Analysis of Pig Muscle Exudate through Label-Free Liquid Chromatography-Mass Spectrometry.Animals : an open access journal from MDPI · 2023Article
- Advances in exercise to alleviate sarcopenia in older adults by improving mitochondrial dysfunction.Frontiers in physiology · 2023Review
- Label-free quantitative proteomics and stress responses in pigs-The case of short or long road transportation.PloS one · 2022Article
- Exercise and mitochondrial mechanisms in patients with sarcopenia.Frontiers in physiology · 2022Review
- Hypoxia and Hypoxia-Inducible Factor Signaling in Muscular Dystrophies: Cause and Consequences.International journal of molecular sciences · 2021Review
- Beneficial Role of Exercise in the Modulation ofAntioxidants (Basel, Switzerland) · 2021Review
- Targeting Nrf2 for the treatment of Duchenne Muscular Dystrophy.Redox biology · 2021Review
- Indices of Defective Autophagy in Whole Muscle and Lysosome Enriched Fractions From Aged D2-mdx Mice.Frontiers in physiology · 2021Article
- Neutralizing mitochondrial ROS does not rescue muscle atrophy induced by hindlimb unloading in female mice.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- Markers of Accelerated Skeletal Muscle Regenerative Response in Murphy Roths Large Mice: Characteristics of Muscle Progenitor Cells and Circulating Factors.Stem cells (Dayton, Ohio) · 2019Article
- Loss of peroxiredoxin-2 exacerbates eccentric contraction-induced force loss in dystrophin-deficient muscle.Nature communications · 2018Article
- Utrophin influences mitochondrial pathology and oxidative stress in dystrophic muscle.Skeletal muscle · 2017Article
- Control of DNA integrity in skeletal muscle under physiological and pathological conditions.Cellular and molecular life sciences : CMLS · 2017Review
- Oral quercetin administration transiently protects respiratory function in dystrophin-deficient mice.The Journal of physiology · 2016Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
It has been well established that oxidative stress contributes to pathology associated with Duchenne muscular dystrophy (DMD). I hypothesized that overexpression of the antioxidant enzyme catalase would improve muscle function in the mdx mouse, the mouse model of DMD. To test this hypothesis, neonatal mdx mice were injected with a recombinant adeno-associated virus driving the catalase transgene. Animals were killed 4 or 6 weeks or 6 months following injection. Muscle function was generally improved by catalase overexpression. Four weeks following injection, extensor digitorum longus specific tension was improved twofold, while soleus was similar between groups. Resistance to contraction-induced injury was similar between groups; however, resistance to fatigue was increased 25% in catalase-treated soleus compared with control muscle. Six weeks following injection, extensor digitorum longus specific tension was increased 15%, while soleus specific tension was similar between treated and untreated limbs. Catalase overexpression reduced contraction-induced injury by 30-45% and fatigue by 20% compared with control limbs. Six months following injection, diaphragm specific tension was similar between groups, but resistance to contraction-induced injury was improved by 35% and fatigue by 25%. Taken together, these data indicate that catalase can improve a subset of parameters of muscle function in dystrophin-deficient skeletal muscle.
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Registered trials
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