ArticleJCSM rapid communications
Overexpression of thioredoxin-2 attenuates age-related muscle loss by suppressing mitochondrial oxidative stress and apoptosis.
Article in JCSM rapid communications. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Human P53 Expression in Yeast: Investigating Its Apoptotic Effects.Mini reviews in medicinal chemistry · 2026Review
- A Reassessment of Sarcopenia from a Redox Perspective as a Basis for Preventive and Therapeutic Interventions.International journal of molecular sciences · 2025Review
- Thiosulphate sulfurtransferase: Biological roles and therapeutic potential.Redox biology · 2025Review
- Thiosulfate sulfurtransferase deficiency promotes oxidative distress and aberrant NRF2 function in the brain.Redox biology · 2023Article
- Pulsed Electromagnetic Fields Induce Skeletal Muscle Cell Repair by Sustaining the Expression of Proteins Involved in the Response to Cellular Damage and Oxidative Stress.International journal of molecular sciences · 2023Article
- Article
- Overexpression of thioredoxin-2 attenuates age-related muscle loss by suppressing mitochondrial oxidative stress and apoptosis.JCSM rapid communicationsArticle
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Authors and funding
19 authors.
Funding
Abstract
Background: Skeletal muscle mass is regulated by intracellular anabolic and catabolic activities. Increased catabolic activity can shift the balance towards net protein breakdown and muscle atrophy. Mitochondrial oxidative stress activates catabolism and is linked to muscle loss. Reducing mitochondrial oxidative stress is thus a plausible approach to prevent muscle atrophy. We tested this concept in age-dependent muscle atrophy by genetically overexpressing the mitochondrial antioxidant thioredoxin-2 (TXN2). Methods: We tested the functional role of TXN2 using ageing ( Results: Overexpression of TXN2 did not significantly alter the baseline skeletal muscle size, weight, fibre type distribution, or expression of mitochondrial respiratory chain components, but it did preserve muscle mass during ageing. The hindlimb muscle mass in aged TXN-transgenic mice was ~21-24% greater (in tibialis anterior, gastrocnemius/soleus combined, and tibialis anterior/extensor digitorum longus combined) than in age-matched controls (all Conclusions: Mitochondrial oxidative stress appears to play a crucial role in effecting chronic age-dependent, but not acute neurogenic, muscle atrophy. Increased TXN2 protects muscle against oxidative stress-associated catabolic activity in ageing muscle and thus is a potential therapeutic approach to attenuate age-related muscle atrophy.
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