Ca2+/calmodulin-dependent protein kinase II equally induces sarcoplasmic reticulum Ca2+ leak in human ischaemic and dilated cardiomyopathy
Ca2+/calmodulin-dependent protein kinase II equally induces sarcoplasmic reticulum Ca2+ leak in human ischaemic and dilated cardiomyopathy
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DOI：
10.1002/ejhf.163
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发表时间：
2014-12-01
影响因子：
18.2
通讯作者：
Sossalla, Samuel
中科院分区：
文献类型：
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作者：
Fischer, Thomas H.;Eiringhaus, Joerg;Sossalla, Samuel
目的肌浆网Ca2+渗漏是心衰（HF）的重要病理机制。研究表明，Ca2+/钙调素依赖性蛋白激酶II （CaMKII）仅与非缺血性HF中SR Ca2+泄漏的诱导相关，而与缺血性HF无关。因此，我们研究了CaMKII及其靶点，以及CaMKII抑制在人缺血性心肌病（ICM, n=37）和扩张型心肌病（DCM, n=40）中的功能作用。方法和结果western blot结果显示，Thr286的表达（增加549%）和自磷酸化(增加129 +/- 29%，P
AimsThe sarcoplasmic reticulum (SR) Ca2+ leak is an important pathomechanism in heart failure (HF). It has been suggested that Ca2+/calmodulin-dependent protein kinase II (CaMKII) is only relevant for the induction of the SR Ca2+ leak in non-ischaemic but not in ischaemic HF. Therefore, we investigated CaMKII and its targets as well as the functional effects of CaMKII inhibition in human ischaemic cardiomyopathy (ICM, n=37) and dilated cardiomyopathy (DCM, n=40).Methods and resultsWestern blots showed a significantly increased expression (by 549%) and autophosphorylation at Thr286 (by 129 +/- 29%, P