CaMKII inhibition protects against hyperthyroid arrhythmias and adverse myocardial remodeling
CaMKII inhibition protects against hyperthyroid arrhythmias and adverse myocardial remodeling
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CaMKII 抑制可预防甲状腺功能亢进性心律失常和不良心肌重塑
DOI：
10.1016/j.bbrc.2022.04.082
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发表时间：
2022
影响因子：
3.1
通讯作者：
Jingdong Li
中科院分区：
文献类型：
--
作者：
Daan Nie;Chaorui Xia;Zhiyu Wang;Peiwu Ding;Yidi Meng;Jie Liu;Ting Li;Ting Gan;Baijun Xuan;Yun Huang;Jiaming Zhang;Guanhua Su;Jingdong Li
甲亢可加重心律失常和心肌肥厚，而钙/钙调蛋白依赖性激酶II(CaMKII)则促进非适应性心肌重塑。然而，目前尚不清楚CaMKII是否有助于甲亢性心脏病(HHD)的进展。本研究证明，抑制CaMKII可以减轻心功能正常的甲亢小鼠的不良心肌重构，减少窦性心动过速、异丙肾上腺素诱发的房颤和室性心律失常。CaMKII上调诱导的HDAC4/MEF2a活化可促进甲亢性心肌肥大。简而言之，抑制CaMKII通过预防心律失常和适应性不良重塑，极大地有利于HHD的治疗。
Hyperthyroidism can potentiate arrhythmias and cardiac hypertrophy, whereas Ca2+/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.