Objective: To investigate the changes of ryanodine receptor 2 (RyR2) mRNA expression in rats suffering from acute myocardial ischemia.
Methods: SD rats were divided randomly into normal control group, myocardial ischemia group and sudden death group. The models of myocardial ischemia and sudden cardiac death were induced by intraperitoneal injection of hypophysine. The changes of RyR2 mRNA expression in cardiac sarcoplasmic reticulum (SR) of rats suffering from myocardial ischemia were detected by fluorescent RT-PCR technique.
Results: The levels of RyR2 mRNA in the myocardial ischemia group and sudden death group were significant lower than those in the control group (P<0.05).
Conclusion: Myocardial ischemia may induce down-regulation of cardiac SR RyR2 mRNA expression.
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Calcium handling abnormalities increase arrhythmia susceptibility in DMSXL myotonic dystrophy type 1 mice.
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Cardiovascular Research Program, VA New York Harbor Healthcare System, New York, NY, USA; Department of Medicine, Cell Biology and Pharmacology, State University of New York Downstate Health Sciences University, New York, NY, USA; Department of Medicine, NYU Langone School of Medicine, New York, NY, USA. Electronic address:
Background: Myotonic dystrophy type 1 (DM1) is a multiorgan disorder with significant cardiac involvement. ECG abnormalities, including arrhythmias, occur in 80 % of DM1 patients and are the second-most common cause of death after respiratory complications; however, the mechanisms underlying the arrhythmogenesis remain unclear. The objective of this study was to investigate the basis of the electrophysiological abnormalities in DM1 using the DMSXL mouse model.
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Int J Mol Sci
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Division of Cardiovascular Sciences, The University of Manchester, Manchester M13 9PL, UK.
(1) Background: The sinus node (SN) is the main pacemaker of the heart. It is characterized by pacemaker cells that lack mitochondria and contractile elements. We investigated the possibility that transcription factors (TFs) and microRNAs (miRs) present in the SN can regulate gene expression that affects SN morphology and function.
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Comp Biochem Physiol C Toxicol Pharmacol
September 2024
Department of Ocean Integrated Science, Chonnam National University, Yeosu 59626, South Korea; Fisheries Science Institute, Chonnam National University, Yeosu 59626, South Korea. Electronic address:
Endocrine-disrupting chemicals (EDCs) are toxic pollutants generated by artificial activities. Moreover, their hormone-like structure induces disturbances, such as mimicking or blocking metabolic activity. Previous studies on EDCs have focused on the adverse effect of the endocrine system in vertebrates, with limited investigations conducted on ion channels in invertebrates.
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Heart Rhythm
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