ArticleMolecular metabolism2019
α-Calcitonin gene-related peptide inhibits autophagy and calpain systems and maintains the stability of neuromuscular junction in denervated muscles.
Article in Molecular metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Clinical and early biochemical responses to botulinum toxin type-A in refractory masticatory myofascial pain: a pilot single-arm study.BMC oral health · 2026Article
- Exploring the effects of lifelong aerobic exercise on early skeletal muscle remodeling between 8 and 14 months in the rat.Journal of physiology and biochemistry · 2026Article
- Aging induces sarcopenia by disrupting the crosstalk between the skeletal muscle microenvironment and myofibers.Journal of advanced research · 2026Review
- Molecular interaction mechanisms of muscle fiber type transition in aging sarcopenia and the role of exercise intervention.The Egyptian journal of internal medicine · 2026Article
- Age, cancer, and the dual burden of cancer and doxorubicin in skeletal muscle wasting in female rats: which one to blame?Biogerontology · 2025Article
- AMPK/MTOR/TP53 Signaling Pathway Regulation by Calcitonin Gene-Related Peptide Reduces Oxygen-Induced Lung Damage in Neonatal Rats through Autophagy Promotion.Inflammation · 2024Article
- Sympathetic innervation in skeletal muscle and its role at the neuromuscular junction.Journal of muscle research and cell motility · 2024Review
- The roles of autophagy and mitophagy in corneal pathology: current knowledge and future perspectives.Frontiers in medicine · 2023Review
- MiR-142a-3p: A novel ACh receptor transcriptional regulator in association with peripheral nerve injury.Molecular therapy. Nucleic acids · 2022Article
- Functional Nutrients to Ameliorate Neurogenic Muscle Atrophy.Metabolites · 2022Review
- A neuromuscular perspective of sarcopenia pathogenesis: deciphering the signaling pathways involved.GeroScience · 2022Article
- The emerging role of the sympathetic nervous system in skeletal muscle motor innervation and sarcopenia.Ageing research reviews · 2021Review
- Denervation-Related Neuromuscular Junction Changes: From Degeneration to Regeneration.Frontiers in molecular neuroscience · 2021Review
- Sarcopenia: What Is the Origin of This Aging-Induced Disorder?Frontiers in genetics · 2021Review
- Regulatory Function of Sympathetic Innervation on the Endo/Lysosomal Trafficking of Acetylcholine Receptor.Frontiers in physiology · 2021Article
- The TOR Pathway at the Neuromuscular Junction: More Than a Metabolic Player?Frontiers in molecular neuroscience · 2020Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveAlthough it is well established that a-calcitonin gene-related peptide (CGRP) stabilizes muscle-type cholinergic receptors nicotinic subunits (AChR), the underlying mechanism by which this neuropeptide regulates muscle protein metabolism and neuromuscular junction (NMJ) morphology is unclear.
methodsTo elucidate the mechanisms how CGRP controls NMJ stability in denervated mice skeletal muscles, we carried out physiological, pharmacological, and molecular analyses of atrophic muscles induced by sciatic nerve transection.
resultsHere, we report that CGRP treatment in vivo abrogated the deleterious effects on NMJ upon denervation (DEN), an effect that was associated with suppression of skeletal muscle proteolysis, but not stimulation of protein synthesis. CGRP also blocked the DEN-induced increase in endocytic AChR vesicles and the elevation of autophagosomes per NMJ area. The treatment of denervated animals with rapamycin blocked the stimulatory effects of CGRP on mTORC1 and its inhibitory actions on autophagic flux and NMJ degeneration. Furthermore, CGRP inhibited the DEN-induced hyperactivation of Ca
conclusionTaken together, these data suggest that the inhibitory effect of CGRP on autophagy and calpain may represent an important mechanism for the preservation of synapse morphology when degradative machinery is exacerbated upon denervation conditions.
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