Ca2+/钙调素依赖性蛋白激酶II在心力衰竭中的作用

Howard Schulman , Mark E. Anderson
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引用次数: 26

摘要

Ca2+/calmodulin (CaM)依赖性蛋白激酶II (CaMKII)现在被认为在心肌生物学和疾病中发挥核心作用。CaMKII似乎通过催化参与心脏兴奋-收缩偶联的主要蛋白的磷酸化来分级心肌性能和调节心率。在病理性应激下,CaMKII激活肥大和炎症转录途径,促进细胞凋亡。动物研究表明,抑制CaMKII可能是治疗常见形式的结构性心脏病的有效方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Ca2+/calmodulin-dependent protein kinase II in heart failure

Ca2+/calmodulin-dependent protein kinase II in heart failure

Ca2+/calmodulin-dependent protein kinase II in heart failure

Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII) is now recognized to play a central role in myocardial biology and disease. CaMKII appears to grade myocardial performance and regulate heart rate by catalyzing the phosphorylation of major proteins involved in cardiac excitation-contraction coupling. Under pathological stress, CaMKII activates hypertrophic and inflammatory transcriptional pathways and promotes apoptosis. Animal studies suggest that CaMKII inhibition may be an effective approach for treating common forms of structural heart disease.

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