![]() found that exposure to constant light contributed to damage of cardiac Cx43 channels‐mediated electrical communication in rats, thereby increasing the risk of malignant cardiac arrhythmias. 9 Increasing evidence showed that preventing the opening of Cx43 hemichannels had a protective effect against I/R injury. 7, 8 If the activation of hemichannels was uncontrolled, significant changes may be caused in cardiomyocyte homeostasis, leading to dysfunction and ultimately irreversible injury in the heart. 6 Hemichannels are often regarded as “pathologic pores” that open abnormally in response to cellular stress. 5 Connexin 43 (Cx43), a member of the connexins, is a special GJ protein that is most abundant on the cell membrane of mammalian ventricular cardiomyocytes. 4 Therefore, how to alleviate susceptibility to RA and protect myocardial functions effectively is always a hot spot in clinical research.Įlectrophysiological remodeling during I/R‐related arrhythmia is, in part, owing to cardiac gap junction (GJ) (fluorescence) uncoupling, and the eventual cellular injury can be determined by the acute effects of the passage of cell‐survival or apoptotic signals through open GJ channels between contiguous myocytes. 3 Reperfusion therapy‐related arrhythmia has conferred an independent mortality risk factor. 2 The most common manifestations of reperfusion arrhythmia (RA) are ventricular tachycardia and ventricular fibrillation (VF), which can lead to hemodynamic disorders and even sudden cardiac death. ![]() 1 MIRI can prolong action potential duration and QT interval, and these electrophysiological changes increase the risk of the myocardium to arrhythmia. Myocardial ischemia/reperfusion (I/R) injury (MIRI) refers to a phenomenon wherein the restoration of blood supply to the myocardium after ischemia does not improve cardiac function but leads to secondary tissue damage.
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