ArticleHuman molecular genetics2013
Transient systemic mtDNA damage leads to muscle wasting by reducing the satellite cell pool.
Article in Human molecular genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 56 citations in OpenAlex.
- Impaired Complex I dysregulates neural/glial precursors and corpus callosum development revealing postnatal defects in Leigh syndrome mice.EMBO molecular medicine · 2026Article
- Basal metabolic rate predicts dementia in community-dwelling older adults: a 5-year longitudinal study.European geriatric medicine · 2025Article
- Impact of exercise-induced DNA damage repair on age-related muscle weakness and sarcopenia.Frontiers in genetics · 2025Review
- Xenogeneic transplantation of mitochondria induces muscle regeneration in an in vivo rat model of dexamethasone-induced atrophy.Journal of muscle research and cell motility · 2024Article
- Emerging roles of mitochondrial functions and epigenetic changes in the modulation of stem cell fate.Cellular and molecular life sciences : CMLS · 2024Review
- Emerging Multi-omic Approaches to the Molecular Diagnosis of Mitochondrial Disease and Available Strategies for Treatment and Prevention.Current genomics · 2024Review
- Relationship between muscle mass and muscle strength with physical performance in older adults: A systematic review.SAGE open medicine · 2023Review
- Pharmaceutical Agents for Contractile-Metabolic Dysfunction After Volumetric Muscle Loss.Tissue engineering. Part A · 2022Article
- Role of Myostatin in Muscle Degeneration by Random Positioning Machine Exposure: AnFrontiers in physiology · 2022Article
- The Association of Mitochondrial Copy Number With Sarcopenia in Adult Survivors of Childhood Cancer.Journal of the National Cancer Institute · 2021Article
- Age-Related Alterations at Neuromuscular Junction: Role of Oxidative Stress and Epigenetic Modifications.Cells · 2021Review
- p53 is required for nuclear but not mitochondrial DNA damage-induced degeneration.Cell death & disease · 2021Article
- Mitochondria and autophagy in adult stem cells: proliferate or differentiate.Journal of muscle research and cell motility · 2020Article
- The mitochondria regulation of stem cell aging.Mechanisms of ageing and development · 2020Review
- Mitochondrial-specific autophagy linked to mitochondrial dysfunction following traumatic freeze injury in mice.American journal of physiology. Cell physiology · 2020Article
- Manipulating and elucidating mitochondrial gene expression with engineered proteins.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Review
- Fis1 deficiencies differentially affect mitochondrial quality in skeletal muscle.Mitochondrion · 2019Article
- Inhibition of ubiquitin-specific protease 2 causes accumulation of reactive oxygen species, mitochondria dysfunction, and intracellular ATP decrement in C2C12 myoblasts.Physiological reports · 2019Article
- Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
With age, muscle mass and integrity are progressively lost leaving the elderly frail, weak and unable to independently care for themselves. Defined as sarcopenia, this age-related muscle atrophy appears to be multifactorial but its definite cause is still unknown. Mitochondrial dysfunction has been implicated in this process. Using a novel transgenic mouse model of mitochondrial DNA (mtDNA) double-strand breaks (DSBs) that presents a premature aging-like phenotype, we studied the role of mtDNA damage in muscle wasting. We caused DSBs in mtDNA of adult mice using a ubiquitously expressed mitochondrial-targeted endonuclease, mito-PstI. We found that a short, transient systemic mtDNA damage led to muscle wasting and a decline in locomotor activity later in life. We found a significant decline in muscle satellite cells, which decreases the muscle's capacity to regenerate and repair during aging. This phenotype was associated with impairment in acetylcholinesterase (AChE) activity and assembly at the neuromuscular junction (NMJ), also associated with muscle aging. Our data suggests that systemic mitochondrial dysfunction plays important roles in age-related muscle wasting by preferentially affecting the myosatellite cell pool.
Indexed as
Identifiers
What OpenQuestion holds
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.