| First Author | Nie D | Year | 2022 |
| Journal | Biochem Biophys Res Commun | Volume | 615 |
| Pages | 136-142 | PubMed ID | 35617800 |
| Mgi Jnum | J:326826 | Mgi Id | MGI:7311167 |
| Doi | 10.1016/j.bbrc.2022.04.082 | Citation | Nie D, et al. (2022) CaMKII inhibition protects against hyperthyroid arrhythmias and adverse myocardial remodeling. Biochem Biophys Res Commun 615:136-142 |
| abstractText | Hyperthyroidism can potentiate arrhythmias and cardiac hypertrophy, whereas Ca(2+)/calmodulin-dependent kinase II (CaMKII) promotes maladaptive myocardial remodeling. However, it remains unclear whether CaMKII contributes to the progression of hyperthyroid heart disease (HHD). This study demonstrated that CaMKII inhibition can relieve adverse myocardial remodeling and reduce sinus tachycardia, isoproterenol-induced atrial fibrillation, and ventricular arrhythmias in hyperthyroid mice with preserved heart function. Hyperthyroid cardiac hypertrophy was promoted by CaMKII upregulation-induced HDAC4/MEF2a activation. Briefly, CaMKII inhibition benefits HHD management greatly in mice by preventing arrhythmias and maladaptive remodeling. |
