ArticleBritish journal of pharmacology2010
Activation of cardiac muscarinic M3 receptors induces delayed cardioprotection by preserving phosphorylated connexin43 and up-regulating cyclooxygenase-2 expression.
Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 54 citations in OpenAlex.
- Research progress in myocardial function and diseases related to muscarinic acetylcholine receptor (Review).International journal of molecular medicine · 2025Review
- Ethanolic Extracts of Cupressaceae Species Conifers Provide Rapid Protection against Barium Chloride-Induced Cardiac Arrhythmia.Pharmaceuticals (Basel, Switzerland) · 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
- Outcomes of hypothalamic oxytocin neuron-driven cardioprotection after acute myocardial infarction.Basic research in cardiology · 2023Article
- The association between RGS4 and choline in cardiac fibrosis.Cell communication and signaling : CCS · 2021Article
- Advances of Traditional Chinese Medicine Regulating Connexin43 in the Prevention and Treatment of Myocardial Infarction.Evidence-based complementary and alternative medicine : eCAM · 2021Review
- 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
- Revisiting the Cardioprotective Effects of Acetylcholine Receptor Activation against Myocardial Ischemia/Reperfusion Injury.International journal of molecular sciences · 2018Review
- Choline ameliorates cardiovascular damage by improving vagal activity and inhibiting the inflammatory response in spontaneously hypertensive rats.Scientific reports · 2017Article
- Vagal nerve stimulation improves mitochondrial dynamics via an MJournal of cellular and molecular medicine · 2017Article
- Novel strategies and underlying protective mechanisms of modulation of vagal activity in cardiovascular diseases.British journal of pharmacology · 2015Review
- Activation of M3 cholinoceptors attenuates vascular injury after ischaemia/reperfusion by inhibiting the Ca2+/calmodulin-dependent protein kinase II pathway.British journal of pharmacology · 2015Article
- Cardiac resynchronization therapy restores sympathovagal balance in the failing heart by differential remodeling of cholinergic signaling.Circulation research · 2015Article
- Altered Connexin 43 and Connexin 45 protein expression in the heart as a function of social and environmental stress in the prairie vole.Stress (Amsterdam, Netherlands) · 2015Article
- Hindlimb unloading results in increased predisposition to cardiac arrhythmias and alters left ventricular connexin 43 expression.American journal of physiology. Regulatory, integrative and comparative physiology · 2013Article
- Choline protects against cardiac hypertrophy induced by increased after-load.International journal of biological sciences · 2013Article
- Choline inhibits angiotensin II-induced cardiac hypertrophy by intracellular calcium signal and p38 MAPK pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeActivation of muscarinic M(3) mucarinic acetylcholine receptors (M(3)-mAChRs) has been previously shown to confer short-term cardioprotection against ischaemic injuries. However, it is not known whether activation of these receptors can provide delayed cardioprotection. Consequently, the present study was undertaken to investigate whether stimulation of M(3)-mAChRs can induce delayed preconditioning in rats, and to characterize the potential mechanism. EXPERIMENTAL APPROACH: Rats were pretreated (24 h), respectively, with M(3)-mAChRs agonist choline, M(3)-mAChRs antagonist 4-DAMP or M(2)-mAChRs antagonist methoctramine followed by the administration of choline. This was followed by 30 min of ischaemia and then 3 h of reperfusion. Ischaemia-induced arrhythmias and ischaemia-reperfusion (I/R)-induced infarction were determined. The phosphorylation status of connexin43 (Cx43) after 30 min ischaemia, and the expression level of Hsp70, cyclooxygenase-2 (COX-2) and iNOS effected by administration of choline were also measured. KEY
resultsCompared to the control group, pretreatment with choline significantly decreased ischaemia-induced arrhythmias, reduced the total number of ventricular premature beats, the duration of ventricular tachycardia episodes and markedly reduced I/R-induced infarct size. Furthermore, choline attenuated ischaemia-induced dephosphorylation of Cx43, and up-regulated the expression of Hsp70 and COX-2. Administration of 4-DAMP abolished these changes, while methoctramine had no effect. CONCLUSIONS AND IMPLICATIONS: Our results suggest that stimulation of M(3)-mAChRs with choline elicits delayed preconditioning, which we propose is the result of up-regulation of the expression of COX-2 and inhibition of the ischaemia-induced dephosphorylation of Cx43. Therefore, M(3)-mAChRs represent a promising target for rendering cardiomyocytes tolerant to ischaemic injury.
Indexed as
Identifiers
What OpenQuestion holds
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.