ArticleJournal of translational medicine2013
Upregulation of M₃ muscarinic receptor inhibits cardiac hypertrophy induced by angiotensin II.
Article in Journal of translational medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- Regulation of mechanical intercellular junctions and components of the mitochondrial electron transport chain and the TCA cycle in the hypertrophic heart by pyridostigmine or trandolapril.Frontiers in molecular biosciences · 2026Article
- Article
- Review
- The Role of Muscarinic Acetylcholine Receptor MInternational journal of molecular sciences · 2024Review
- Muscarinic Receptors in Cardioprotection and Vascular Tone Regulation.Physiological research · 2024Review
- Pathophysiology and pharmacology of G protein-coupled receptors in the heart.Cardiovascular research · 2023Review
- Review
- Acetylcholine exerts cytoprotection against hypoxia/reoxygenation-induced apoptosis, autophagy and mitochondrial impairment through both muscarinic and nicotinic receptors.Apoptosis : an international journal on programmed cell death · 2022Article
- Pharmacological Modulation of Vagal Nerve Activity in Cardiovascular Diseases.Neuroscience bulletin · 2019Review
- The attenuation of myocardial hypertrophy by atorvastatin via the intracellular calcium signal and the p38 MAPK pathway.International journal of clinical and experimental pathology · 2019Article
- Choline Attenuates Cardiac Fibrosis by Inhibiting p38MAPK Signaling Possibly by Acting on MFrontiers in pharmacology · 2019Article
- Revisiting the Cardioprotective Effects of Acetylcholine Receptor Activation against Myocardial Ischemia/Reperfusion Injury.International journal of molecular sciences · 2018Review
- Cholinergic activity as a new target in diseases of the heart.Molecular medicine (Cambridge, Mass.) · 2015Review
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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
backgroundM₃ muscarinic acetylcholine receptor (M₃-mAChR) is stably expressed in the myocardium, but its pathophysiological role remains largely undefined. This study aimed to investigate the role of M₃-mAChR in cardiac hypertrophy induced by angiotensin II (Ang II) and elucidate the underlying mechanisms.
methodsCardiac-specific M₃-mAChR overexpression transgenic (TG) mice and rat H9c2 cardiomyoblasts with ectopic expression of M₃-mAChR were established. Models of cardiac hypertrophy were induced by transverse aortic constriction (TAC) or Ang II infusion in the mice in vivo, and by isoproterenol (ISO) or Ang II treatment of H9c2 cells in vitro. Cardiac hypertrophy was evaluated by electrocardiography (ECG) measurement, hemodynamic measurement and histological analysis. mRNA and protein expression were detected by real-time RT-PCR and Western blot analysis.
resultsM₃-mAChR was upregulated in hypertrophic heart, while M₂-mAChR expression did not change significantly. M₃-mAChR overexpression significantly attenuated the increased expression of atrial natriuretic peptide and β-myosin heavy chain induced by Ang II both in vivo and in vitro. In addition, M₃-mAChR overexpression downregulated AT1 receptor expression and inhibited the activation of MAPK signaling in the heart.
conclusionThe upregulation of M₃-mAChR during myocardial hypertrophy could relieve the hypertrophic response provoked by Ang II, and the mechanism may involve the inhibition of MAPK signaling through the downregulation of AT1 receptor.
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