The reduction in hypothermia and ischaemia-induced reperfusion arrhythmias by the addition of sevoflurane to HTK solution may be related to the phosphorylation of Cx43 at serine 368.
However, enhanced phosphorylation of Cx43 at serine368 in hypothyroid SHRs might be associated with preservation of intercellular coupling and alleviation of the propensity of the heart to malignant arrhythmias.
These results supported that inhibition of miR-206 ameliorates ischemia-reperfusion arrhythmia by targeting Cx43, and this miR-206/Cx43 axis could serve as a potential target for the management of ischemic-perfusion arrhythmia.
We have shown previously that during myocardial ischemia/reperfusion (MI/R), toll-like receptor 2 (TLR2) signaling regulates connexin 43 (Cx43) subcellular localization and function and dampens arrhythmia formation.
The potential impact of these findings may be considerable, and suggests that high-sucrose intake impairs myocardial signaling mediated by Cx43 and PKC contributing to increased susceptibility of the older obese female rat hearts to malignant arrhythmias.
Our results demonstrate that opening of remodeled and S-nitrosylated Cx43 hemichannels play a key role in the development of arrhythmias in DMD mice and may serve as therapeutic targets to prevent fatal arrhythmias in DMD patients.
Cardiomyocytes of diabetic <i>Adamts13</i><sup>-/-</sup> mice exhibited an aberrant distribution of the ventricular gap junction connexin 43 and increased phosphorylation of Ca<sup>2+</sup>/calmodulin-dependent kinase II (CaMKII), and with the consequent CaMKII-induced disturbance in Ca<sup>2+</sup> handling, which underlie propensity for arrhythmia.
Studies in wild-type and transgenic mice indicate that enhanced CK1-phosphorylation of Cx43 protects from arrhythmia, while dephosphorylation precedes arrhythmia vulnerability.
Cx43 was expressed in (myo)fibroblasts and CD45<sup>+</sup> cells within the scar and provided prominent and long lasting arrhythmia protection in vivo.
We conclude that sEHIs can repress miR-1, thus stimulate expression of <i>KCNJ2</i>/Kir2.1 and <i>GJA1</i>/Cx43 mRNA/protein in MI mice, suggesting a possible mechanism for its potential therapeutic application in ischemic arrhythmias.
Downregulation of Cx43 (connexin 43), the major cardiac gap junction protein, is often associated with arrhythmia, dilated cardiomyopathy (DCM), and heart failure.
Altered thyroid status affects myocardial expression of connexin-43 and susceptibility of rat heart to malignant arrhythmias that can be partially normalized by red palm oil intake.
To observe the expressions of myocardial connexin43 (Cx43) and interleukin-17 (IL-17) in acute myocardial infarction (AMI) rats and investigate its possible mechanism of telmisartan in the prevention and treatment of arrhythmia in AMI.
The Cx43D378stop mice reveal for the first time that Cx43 dependent arrhythmias can develop by mechanisms other than impairment of gap junction channel function.
Recent studies have reported an association between nucleotide substitutions in the connexin40 (Cx40) and connexin43 (Cx43) genes (GJA5 and GJA1, respectively) and cardiac arrhythmias.