ArticleAutophagy2017
Suppression of CHRN endocytosis by carbonic anhydrase CAR3 in the pathogenesis of myasthenia gravis.
Article in Autophagy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Comprehensive transcriptomic profiling reveals impaired polyamine metabolism as a contributor to age-related muscle decline.iScience · 2026Article
- HMGB1-mediated endoplasmic reticulum stress in monocyte-derived dendritic cells regulates CD4+ T cell immune responses in myasthenia gravis.Journal of neuroinflammation · 2026Article
- Carbonic Anhydrase 3 Overexpression Modulates Signalling Pathways Associated with Cellular Stress Resilience and Proteostasis.International journal of molecular sciences · 2025Article
- Astrocyte Autophagy in Neurodegenerative Diseases: Current Progress in Mechanisms and Therapeutics.Neurochemical research · 2025Review
- Interactions Between Extracellular Vesicles and Autophagy in Neuroimmune Disorders.Neuroscience bulletin · 2024Review
- Gut microbiota-derived butyrate restores impaired regulatory T cells in patients with AChR myasthenia gravis via mTOR-mediated autophagy.Cell communication and signaling : CCS · 2024Article
- Carbonic Anhydrase 3 is required for cardiac repair post myocardial infarction via Smad7-Smad2/3 signaling pathway.International journal of biological sciences · 2024Article
- Modulation of cardiac resident macrophages immunometabolism upon high-fat-diet feeding in mice.Frontiers in immunology · 2024Article
- PAI1 inhibits the pathogenesis of primary focal hyperhidrosis by targeting CHRNA1.Orphanet journal of rare diseases · 2023Article
- A multilevel screening pipeline in zebrafish identifies therapeutic drugs for GAN.EMBO molecular medicine · 2023Article
- Photoactivated adenylyl cyclases attenuate sepsis-induced cardiomyopathy by suppressing macrophage-mediated inflammation.Frontiers in immunology · 2022Article
- Cholino-ncRNAs modulate sex-specific- and age-related acetylcholine signals.FEBS letters · 2020Review
- Proximity-dependent biotinylation screening identifies NbHYPK as a novel interacting partner of ATG8 in plants.BMC plant biology · 2019Article
- mTOR Modulates Methamphetamine-Induced Toxicity through Cell Clearing Systems.Oxidative medicine and cellular longevity · 2018Article
- The Human Carbonic Anhydrase II in Platelets: An Underestimated Field of Its Activity.BioMed research international · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myasthenia gravis is an autoimmune disorder of the neuromuscular junction manifested as fatigable muscle weakness, which is typically caused by pathogenic autoantibodies against postsynaptic CHRN/AChR (cholinergic receptor nicotinic) in the endplate of skeletal muscle. Our previous studies have identified CA3 (carbonic anhydrase 3) as a specific protein insufficient in skeletal muscle from myasthenia gravis patients. In this study, we investigated the underlying mechanism of how CA3 insufficiency might contribute to myasthenia gravis. Using an experimental autoimmune myasthenia gravis animal model and the skeletal muscle cell C2C12, we find that inhibition of CAR3 (the mouse homolog of CA3) promotes CHRN internalization via a lipid raft-mediated pathway, leading to accelerated degradation of postsynaptic CHRN. Activation of CAR3 reduces CHRN degradation by suppressing receptor endocytosis. CAR3 exerts this effect by suppressing chaperone-assisted selective autophagy via interaction with BAG3 (BCL2-associated athanogene 3) and by dampening endoplasmic reticulum stress. Collectively, our study illustrates that skeletal muscle cell CAR3 is critical for CHRN homeostasis in the neuromuscular junction, and its deficiency leads to accelerated degradation of CHRN and development of myasthenia gravis, potentially revealing a novel therapeutic approach for this disorder.
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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.