ArticleMolecular medicine (Cambridge, Mass.)2011
Overexpression of M₃ muscarinic receptor is a novel strategy for preventing sudden cardiac death in transgenic mice.
Article in Molecular medicine (Cambridge, Mass.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Research progress in myocardial function and diseases related to muscarinic acetylcholine receptor (Review).International journal of molecular medicine · 2025Review
- Transcutaneous Auricular Vagus Nerve Stimulation Ameliorates Preeclampsia-Induced Apoptosis of Placental Trophoblastic Cells Via Inhibiting the Mitochondrial Unfolded Protein Response.Neuroscience bulletin · 2024Article
- The Role of Muscarinic Acetylcholine Receptor MInternational journal of molecular sciences · 2024Review
- Muscarinic Receptors in Cardioprotection and Vascular Tone Regulation.Physiological research · 2024Review
- MCardiovascular diagnosis and therapy · 2024Article
- Pathophysiology and pharmacology of G protein-coupled receptors in the heart.Cardiovascular research · 2023Review
- The role of M3 receptors in regulation of electrical activity deteriorates in the rat heart during ageing.Current research in physiology · 2022Article
- Pharmacological Modulation of Vagal Nerve Activity in Cardiovascular Diseases.Neuroscience bulletin · 2019Review
- Choline Attenuates Cardiac Fibrosis by Inhibiting p38MAPK Signaling Possibly by Acting on MFrontiers in pharmacology · 2019Article
- The impact of dual bronchodilation on cardiovascular serious adverse events and mortality in COPD: a quantitative synthesis.International journal of chronic obstructive pulmonary disease · 2017Review
- Tiotropium formulations and safety: a network meta-analysis.Therapeutic advances in drug safety · 2017Article
- Novel strategies and underlying protective mechanisms of modulation of vagal activity in cardiovascular diseases.British journal of pharmacology · 2015Review
- Upregulation of M₃ muscarinic receptor inhibits cardiac hypertrophy induced by angiotensin II.Journal of translational medicine · 2013Article
- Mechanisms underlying the autonomic modulation of ventricular fibrillation initiation--tentative prophylactic properties of vagus nerve stimulation on malignant arrhythmias in heart failure.Heart failure reviews · 2013Review
- Arrhythmogenesis toxicity of aconitine is related to intracellular ca(2+) signals.International journal of medical sciences · 2013Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study was designed to investigate the cardiac benefits of M₃ muscarinic receptor (M₃-mAChR) overexpression and whether these effects are related to the regulation of the inward rectifying K⁺ channel by microRNA-1 (miR-1) in a conditional overexpression mouse model. A cardiac-specific M₃-mAChR transgenic mouse model was successfully established for the first time in this study using microinjection, and the overexpression was confirmed by both reverse transcriptase-polymerase chain reaction and Western blot techniques. We demonstrated that M₃-mAChR overexpression dramatically reduced the incidence of arrhythmias and decreased the mortality in a mouse model of myocardial ischemia-reperfusion (I/R). By using whole-cell patch techniques, M₃-mAChR overexpression significantly shortened the action potential duration and restored the membrane repolarization by increasing the inward rectifying K⁺ current. By using Western blot techniques, M₃-mAChR overexpression also rescued the expression of the inward rectifying K⁺ channel subunit Kir2.1 after myocardial I/R injury. This result was accompanied by suppression of upregulation miR-1. We conclude that M₃-mAChR overexpression reduced the incidence of arrhythmias and mortality after myocardial I/R by protecting the myocardium from ischemia in mice. This effect may be mediated by increasing the inward rectifying K⁺ current by downregulation of arrhythmogenic miR-1 expression, which might partially be a novel strategy for antiarrhythmias, leading to sudden cardiac death.
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