ArticleExperimental and therapeutic medicine2018
Metoprolol protects cardiomyocytes in rabbit model of heart failure by regulating Cx43.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Post translational modifications of connexin 43 in ventricular arrhythmias after myocardial infarction.Molecular biology reports · 2024Review
- Metoprolol Protects Against Arginine Vasopressin-Induced Cellular Senescence in H9C2 Cardiomyocytes by Regulating the Sirt1/p53/p21 Axis.Cardiovascular toxicology · 2022Article
- Caduet enhances connexin 43 phosphorylation in left ventricular and thoracic aorta of SH model rats.Experimental and therapeutic medicine · 2020Article
- Anti-Arrhythmic Effects of LinaloolFrontiers in pharmacology · 2020Article
- Combination of HGF and IGF-1 promotes connexin 43 expression and improves ventricular arrhythmia after myocardial infarction through activating the MAPK/ERK and MAPK/p38 signaling pathways in a rat model.Cardiovascular diagnosis and therapy · 2019Article
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Authors and funding
3 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
This study investigated the protective effect of metoprolol on cardiomyocytes in rabbits with heart failure and its possible mechanism. Sixty New Zealand white rabbits were randomly divided into infarction group and non-infarction group, 30 in each group. Myocardial infarction was constructed by ligation of anterior descending branch of coronary artery. Coronary artery threading without ligation after thoracotomy was performed for rabbits in non-infarction group. After model construction, rabbits in each group were further divided into control group (n=15) and metoprolol group (n=15), and fed with normal diet and normal diet + metoprolol. Animals were sacrificed 8 weeks later, and ventricular tissue around infarction area was collected. Expression of connexin 43 (Cx43) in myocardium was detected by immunohistochemistry. Expression of Cx43 protein and mRNA in each group was detected by western blot and reverse transcription PCR. The Cx43 protein was positively expressed in non-infarction group and was evenly distributed in intercellular space. Compared with non-infarction group, expression of Cx43 in infarction group was significantly decreased or even disappeared, while the decrease in expression level of Cx43 and the degree of dispersion were lower in metoprolol group than in control group. There was no significant difference in expression of level of Cx43 protein and mRNA between the subgroups of non-infarction group (P>0.05). In infarction group, expression level of Cx43 protein and mRNA in the metoprolol group were significantly higher than those in control group (P<0.05). The results showed that metoprolol can protect cardiomyocytes after myocardial infarction, and the possible mechanism is related to the regulation of Cx43 expression in cardiomyocytes.
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