ArticleNature communications2020
Active acetylcholine receptors prevent the atrophy of skeletal muscles and favor reinnervation.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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.
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Who cites it
67 citing papers in PubMed, 109 citations in OpenAlex.
- Trial
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- Mechanotransduction Failure and Molecular Rescue in Gastric Cancer: Kinetotherapy Across the IL-6/STAT3-Myostatin/ACVR2B-Akt/mTOR Axis.Medical sciences (Basel, Switzerland) · 2026Review
- The miR-206-3p/Cpeb1 axis delays acetylcholine receptor degradation and preserves neuromuscular junction stability in denervation-induced muscle atrophy.Cellular and molecular life sciences : CMLS · 2026Article
- Localized Tacrolimus Delivery for Peripheral Nerve Regeneration: Molecular Mechanisms, Biomaterial Platforms, and Translational Strategies.International journal of molecular sciences · 2026Review
- Tanycyte-derived lactate activates astrocytic HCAR1 to modulate glutamatergic signaling and POMC neuron excitability.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Curing the brain: in search for new astrocyte-specific therapies.Experimental & molecular medicine · 2026Review
- New Insights into Neuromuscular Junction Biology: Evidence from Human and Animal Research.International journal of molecular sciences · 2026Review
- Integrative multi-omics and machine learning identify CHRNA1 putative circadian-immune hub in COPD.PloS one · 2026Article
- Zebrafish genetic model of neuromuscular degeneration associated with Atrogin-1 expression.PLoS genetics · 2026Article
- Article
- Structure-based virtual screening for selective connexin hemichannel blockers: a historical perspective on the discovery of a small organic inhibitor.Frontiers in pharmacology · 2026Article
- Exogenous nanomolar zinc ion (ZnBiometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025Article
- Novel Biomolecule-Infused Gelatin Injectable for Treatment of Recurrent Laryngeal Nerve Injury.The Laryngoscope · 2025Article
- Frequency-Dependent Mechanism of 24-Hydroxycholesterol-Mediated Modulation of Neurotransmitter Release at the Mouse Neuromuscular Junction: The Role of Reactive Oxygen Species.Neurochemical research · 2025Article
- Cholesterol-Lowering Treatment Suppresses Neuromuscular Transmission Via Presynaptic Mechanism at the Mouse Diaphragm Muscle.Neurochemical research · 2025Article
- Engineering the Future of Restorative Clinical Peripheral Nerve Surgery.Advanced healthcare materials · 2025Review
- 25-Hydroxycholesterol as a negative regulator of diaphragm muscle contractions via estrogen receptor and CaHistochemistry and cell biology · 2025Article
- Treatment of Denervated Muscle Atrophy by Injectable Dual-Responsive Hydrogels Loaded with Extracellular Vesicles.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
7 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
14 authors at 9 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Denervation of skeletal muscles induces severe muscle atrophy, which is preceded by cellular alterations such as increased plasma membrane permeability, reduced resting membrane potential and accelerated protein catabolism. The factors that induce these changes remain unknown. Conversely, functional recovery following denervation depends on successful reinnervation. Here, we show that activation of nicotinic acetylcholine receptors (nAChRs) by quantal release of acetylcholine (ACh) from motoneurons is sufficient to prevent changes induced by denervation. Using in vitro assays, ACh and non-hydrolysable ACh analogs repressed the expression of connexin43 and connexin45 hemichannels, which promote muscle atrophy. In co-culture studies, connexin43/45 hemichannel knockout or knockdown increased innervation of muscle fibers by dorsal root ganglion neurons. Our results show that ACh released by motoneurons exerts a hitherto unknown function independent of myofiber contraction. nAChRs and connexin hemichannels are potential molecular targets for therapeutic intervention in a variety of pathological conditions with reduced synaptic neuromuscular transmission.
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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.