ArticleJournal of cachexia, sarcopenia and muscle2019
Mitochondrial oxidative stress impairs contractile function but paradoxically increases muscle mass via fibre branching.
Article in Journal of cachexia, sarcopenia and muscle, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 53 papers.
What it found
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Who cites it
53 citing papers in PubMed, 70 citations in OpenAlex.
- Inflammaging-associated mitochondrial degeneration occurs in hypoglossal motor neurons prior to tongue muscle.GeroScience · 2026Article
- Protein arginine methyltransferases coordinate mitochondrial stress adaptation and neuromuscular function.Experimental & molecular medicine · 2026Review
- Unacylated ghrelin counteracts mitochondrial dysfunction and neuromuscular junction disruption in cancer cachexia.American journal of physiology. Cell physiology · 2026Article
- Vitamin D binding protein induces skeletal muscle atrophy and contributes to cancer-associated muscle wasting independently of vitamin D status in preclinical models.Nature communications · 2026Article
- Mitochondrial bioenergetics in resilience of older adults with gynecologic cancer: design and rationale of a pilot study.GeroScience · 2026Article
- Ferroptosis, lipid metabolism, and genetic regulation in postoperative rehabilitation of elderly hip fractures: from molecular mechanisms to clinical translation.Frontiers in genetics · 2026Review
- Muscle Insulin Resistance Elicits Muscle Atrophy in Obesity.Current obesity reports · 2025Review
- Dysferlin and the Regulation of CaCells · 2025Review
- A review: oxidative stress in skeletal muscle and the non-coding RNAs behind it.Molecular and cellular biochemistry · 2025Review
- Article
- Mitochondrial haplotype and sex modulate responses to endurance exercise training.The Journal of physiology · 2025Article
- Reactive oxygen species in the pathogenesis of sarcopenia.Free radical biology & medicine · 2025Review
- Inducible and reversible SOD2 knockdown in mouse skeletal muscle drives impaired pyruvate oxidation and reduced metabolic flexibility.Free radical biology & medicine · 2025Article
- Lipid peroxidation and sarcopenia: molecular mechanisms and potential therapeutic approaches.Frontiers in medicine · 2025Review
- Unacylated Ghrelin Protects Against Age-Related Loss of Muscle Mass and Contractile Dysfunction in Skeletal Muscle.Aging cell · 2024Article
- Mouse models used to test the role of reactive oxygen species in aging and age-related chronic diseases.Free radical biology & medicine · 2024Review
- Inducible and reversible SOD2 knockdown in mouse skeletal muscle drives impaired pyruvate oxidation and reduced metabolic flexibility.bioRxiv : the preprint server for biology · 2024Article
- Transcriptome analysis revealed differences in gene expression in sheep muscle tissue at different developmental stages.BMC genomic data · 2024Article
- How soon do metabolic alterations and oxidative distress precede the reduction of muscle mass and strength in Wistar rats in aging process?Biogerontology · 2024Article
- Senolytic treatment does not mitigate oxidative stress-induced muscle atrophy but improves muscle force generation in CuZn superoxide dismutase knockout mice.GeroScience · 2024Article
Corrections and comments
- Erratum issuedCorrigendum.2019
Authors and funding
20 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundExcess reactive oxygen species (ROS) and muscle weakness occur in parallel in multiple pathological conditions. However, the causative role of skeletal muscle mitochondrial ROS (mtROS) on neuromuscular junction (NMJ) morphology and function and muscle weakness has not been directly investigated.
methodsWe generated mice lacking skeletal muscle-specific manganese-superoxide dismutase (mSod2KO) to increase mtROS using a cre-Lox approach driven by human skeletal actin. We determined primary functional parameters of skeletal muscle mitochondrial function (respiration, ROS, and calcium retention capacity) using permeabilized muscle fibres and isolated muscle mitochondria. We assessed contractile properties of isolated skeletal muscle using in situ and in vitro preparations and whole lumbrical muscles to elucidate the mechanisms of contractile dysfunction.
resultsThe mSod2KO mice, contrary to our prediction, exhibit a 10-15% increase in muscle mass associated with an ~50% increase in central nuclei and ~35% increase in branched fibres (P < 0.05). Despite the increase in muscle mass of gastrocnemius and quadriceps, in situ sciatic nerve-stimulated isometric maximum-specific force (N/cm
conclusionsIncreased skeletal muscle mtROS is sufficient to elicit NMJ disruption and contractile abnormalities, but not muscle atrophy, suggesting new roles for mitochondrial oxidative stress in maintenance of muscle mass through increased fibre branching.
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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.