ArticleProceedings of the National Academy of Sciences of the United States of America2013
Reduced IGF signaling prevents muscle cell death in a Caenorhabditis elegans model of muscular dystrophy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Three muscle-specific DAF-16/FOXO transcriptional targets activated by reduced insulin/IGF-1 signaling.G3 (Bethesda, Md.) · 2026Article
- Cross-species modeling of muscular dystrophy in Caenorhabditis elegans using patient-derived extracellular vesicles.Disease models & mechanisms · 2024Article
- Febuxostat ameliorates muscle degeneration and movement disorder of the dystrophin mutant model in Caenorhabditis elegans.The journal of physiological sciences : JPS · 2023Article
- Spaceflight Induces Strength Decline inCells · 2023Article
- Sulfur amino acid supplementation displays therapeutic potential in a C. elegans model of Duchenne muscular dystrophy.Communications biology · 2022Article
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- Review
- Mitochondrial hydrogen sulfide supplementation improves health in theProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Build-UPS and break-downs: metabolism impacts on proteostasis and aging.Cell death and differentiation · 2021Review
- Chinese liquor extract attenuates oxidative damage in HepG2 cells and extends lifespan ofFood science & nutrition · 2020Article
- Transcriptome changes during the initiation and progression of Duchenne muscular dystrophy in Caenorhabditis elegans.Human molecular genetics · 2020Article
- Alcohol induces mitochondrial fragmentation and stress responses to maintain normal muscle function in Caenorhabditis elegans.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Physical exertion exacerbates decline in the musculature of an animal model of Duchenne muscular dystrophy.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Muscle strength deficiency and mitochondrial dysfunction in a muscular dystrophy model ofDisease models & mechanisms · 2018Article
- UNC-120/SRF independently controls muscle aging and lifespan in Caenorhabditis elegans.Aging cell · 2018Article
- ERG-28 controls BK channel trafficking in the ER to regulate synaptic function and alcohol response ineLife · 2017Article
- Abnormal Osmotic Avoidance Behavior in C. elegans Is Associated with Increased Hypertonic Stress Resistance and Improved Proteostasis.PloS one · 2016Article
- Dystrophin induced cognitive impairment: mechanisms, models and therapeutic strategies.Annals of neurosciences · 2015Review
- The burrowing behavior of the nematode Caenorhabditis elegans: a new assay for the study of neuromuscular disorders.Genes, brain, and behavior · 2015Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Duchenne muscular dystrophy, a fatal degenerative muscle disease, is caused by mutations in the dystrophin gene. Loss of dystrophin in the muscle cell membrane causes muscle fiber necrosis. Previously, loss-of-function mutations in dys-1, the Caenorhabditis elegans dystrophin ortholog, were shown to cause a contractile defect and mild fiber degeneration in striated body wall muscle. Here, we show that loss of dystrophin function in C. elegans results in a shorter lifespan and stochastic, age-dependent muscle-cell death. Reduction of dystrophin function also accelerated age-dependent protein aggregation in muscle cells, suggesting a defect in proteostasis. Both muscle cell death and protein aggregation showed wide variability among the muscle cells. These observations suggest that muscle cell death in dys-1 mutants is greatly influenced by cellular environments. Thus, the manipulation of the cellular environment may provide an opportunity to thwart the cell death initiated by the loss of dystrophin. We found that reduced insulin-like growth factor (IGF) signaling, which rejuvenates the cellular environment to protect cells from a variety of age-dependent pathologies, prevented muscle cell death in the dys-1 mutants in a daf-16-dependent manner. Our study suggests that manipulation of the IGF signaling pathways in muscle cells could be a potent intervention for muscular dystrophy.
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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.