ArticleJCI insight2021
Pancreas-specific CHRM3 activation causes pancreatitis in mice.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- PVNJournal of neuroinflammation · 2026Article
- Intraductal digestive enzyme accumulation drives lethal hemorrhagic necrotizing pancreatitis and enables therapeutic intervention.Research square · 2026Article
- Polymorphism of Melanocortin Receptor Genes-Association with Inflammatory Traits and Diseases.Diseases (Basel, Switzerland) · 2025Review
- Protease Inhibitor VR23 Alleviates Severe Acute Pancreatitis with High Trypsin Synthesis in Mice.Digestive diseases and sciences · 2025Article
- Targeted animal models for preclinical assessment of cellular and gene therapies in pancreatic and liver diseases: regulatory and practical insights.Cytotherapy · 2025Review
- Neuroimmune regulation in the pancreas.Fundamental research · 2024Review
- Galantamine ameliorates experimental pancreatitis.Molecular medicine (Cambridge, Mass.) · 2023Article
- Neural innervation in adipose tissue, gut, pancreas, and liver.Life metabolism · 2023Review
- Multiple roles for cholinergic signaling in pancreatic diseases.World journal of gastroenterology · 2022Review
- Differential Actions of Muscarinic Receptor Subtypes in Gastric, Pancreatic, and Colon Cancer.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
Abstract
Hyperstimulation of the cholecystokinin 1 receptor (CCK1R), a G protein-coupled receptor (GPCR), in pancreatic acinar cells is commonly used to induce pancreatitis in rodents. Human pancreatic acinar cells lack CCK1R but express cholinergic receptor muscarinic 3 (M3R), another GPCR. To test whether M3R activation is involved in pancreatitis, a mutant M3R was conditionally expressed in pancreatic acinar cells in mice. This mutant receptor loses responsiveness to its native ligand, acetylcholine, but can be activated by an inert small molecule, clozapine-N-oxide (CNO). Intracellular calcium and amylase were elicited by CNO in pancreatic acinar cells isolated from mutant M3R mice but not WT mice. Similarly, acute pancreatitis (AP) could be induced by a single injection of CNO in the transgenic mice but not WT mice. Compared with the cerulein-induced AP, CNO caused more widespread acinar cell death and inflammation. Furthermore, chronic pancreatitis developed at 4 weeks after 3 episodes of CNO-induced AP. In contrast, in mice with 3 recurrent episodes of cerulein-included AP, pancreas histology was restored in 4 weeks. Furthermore, the M3R antagonist ameliorated the severity of cerulein-induced AP in WT mice. We conclude that M3R activation can cause the pathogenesis of pancreatitis. This model may provide an alternative approach for pancreatitis research.
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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.