ArticleCell reports2014
Autophagy impairment in muscle induces neuromuscular junction degeneration and precocious aging.
Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 263 papers.
What it found
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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.
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Who cites it
263 citing papers in PubMed, 402 citations in OpenAlex.
- Neuromuscular junctions are stable in patients with cancer cachexia.The Journal of clinical investigation · 2020Trial
- Worse muscle mass loss in adrenal Cushing syndrome vs. Cushing's disease: a comparative evaluation of chemiluminescence and LC-MS/MS cortisol assessment.Journal of endocrinological investigation · 2026Article
- Adding Tat-Beclin1 to an endurance training program promotes additive improvements in physical function in aged male mice.Physiological reports · 2026Article
- The hallmarks of skeletal muscle health.Nature metabolism · 2026Review
- Chronic Contractile Activity Remediates Lysosomal Dysfunction in a Muscle Cell Lysosomal Disease Model.Journal of cellular physiology · 2026Article
- The organellar biology of aging: A mitochondrial vantage.Molecular biology reports · 2026Review
- Immunometabolic Remodeling in Osteosarcopenia: Inflammaging, Mitochondrial Dysfunction, Gut-Derived Metabolites and Therapeutic Opportunities.Metabolites · 2026Review
- Alterations of actin in aging.Journal of cell science · 2026Review
- Effects of empagliflozin alone and in combination with exercise on the soleus muscle in obese type 2 diabetic rats.The journal of physiological sciences : JPS · 2026Article
- Protein arginine methyltransferases coordinate mitochondrial stress adaptation and neuromuscular function.Experimental & molecular medicine · 2026Review
- Transcriptional and epigenetic regulation of autophagy: mechanisms, disease relevance and therapeutic opportunities.Signal transduction and targeted therapy · 2026Review
- Synphilin-1 mitigates autophagy dysfusnction, modulates ubiquitinated protein aggregation, and promotes cell survival during proteotoxic stress.bioRxiv : the preprint server for biology · 2026Article
- Protective effects of irisin in sarcopenia: a promising treatment.Journal of orthopaedic translation · 2026Review
- The Role of Fibro/adipogenic Progenitors (FAPs) in Sarcopenia: Mechanisms and Potential Therapeutic Strategies.Stem cell reviews and reports · 2026Review
- Role of mitochondrial dysfunction in muscle wasting in cancer cachexia: a narrative review.Journal of translational medicine · 2026Review
- Sarcopenia and Muscle Aging: Updated Insights into Molecular Mechanisms and Translational Therapeutics.Endocrinology and metabolism (Seoul, Korea) · 2026Review
- A Validated Transcriptomic NMJ Remodeling Score Reveals Synaptic Dysfunction Independent of Muscle Atrophy after Immobilization in a Microgravity Analog.Neuroinformatics · 2026Article
- Organ-Specific Regulation of Systemic Aging: Focus on the Brain, Skeletal Muscle, and Gut.Cells · 2026Review
- Dietary nitrate supplementation mitigates age-related changes at the neuromuscular junction in mice.The Journal of physiology · 2026Article
- Current Progress in the Role of Ferroptosis in Skeletal Muscle Atrophy.Mediators of inflammation · 2026Review
203 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 10 institutions in 5 countries.
Funding
Abstract
The cellular basis of age-related tissue deterioration remains largely obscure. The ability to activate compensatory mechanisms in response to environmental stress is an important factor for survival and maintenance of cellular functions. Autophagy is activated both under short and prolonged stress and is required to clear the cell of dysfunctional organelles and altered proteins. We report that specific autophagy inhibition in muscle has a major impact on neuromuscular synaptic function and, consequently, on muscle strength, ultimately affecting the lifespan of animals. Inhibition of autophagy also exacerbates aging phenotypes in muscle, such as mitochondrial dysfunction, oxidative stress, and profound weakness. Mitochondrial dysfunction and oxidative stress directly affect acto-myosin interaction and force generation but show a limited effect on stability of neuromuscular synapses. These results demonstrate that age-related deterioration of synaptic structure and function is exacerbated by defective autophagy.
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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.