Matsuo H
Department of Cardiovascular Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
Hokkaido Igaku Zasshi. 1991 May;66(3):348-55.
The creatine kinase system is related to intracellular high-energy phosphate transfer. Mitochondrial creatine kinase catalyzes the transfer of high-energy phosphate between creatine and ATP generated in mitochondria. Creatine phosphate generated in this process is transferred to myofibril. Mitochondrial creatine kinase abnormalities cause the decrease of ATP level in cytoplasm through the disorder of ATP transfer. If such decrease happens in myocardium the depressed cardiac function is suspected. I studied the time course of alterations of the creatine kinase system in BIO14.6 (the model of hypertrophic cardiomyopathy) at 5 weeks, 20 weeks, 50 weeks, and 62 weeks of age, and in BIO53.58 (the model of dilated cardiomyopathy) at 5 weeks and 20 weeks of age. In BIO14.6, creatine kinase activity of myocardium and isolated mitochondria was decreased in 20, 50, 62-week-old hamsters. The share of mitochondrial creatine kinase in the total tissue enzyme activity was decreased, and the share of BB form was increased in 50, 62-week-old hamsters. In BIO53.58, creatine kinase activity of myocardium and isolated mitochondria was decreased in 20-week-old hamsters. The share of mitochondrial creatine kinase was increased, and BB form was decreased in 5, 20-week-old hamsters. The experiments suggest alterations in the creatine kinase system occur at 20 weeks of age in BIO14.6 and at neonatal phase in BIO53.58. These alterations of creatine kinase system may contribute to depressed cardiac function in cardiomyopathy.
肌酸激酶系统与细胞内高能磷酸转移有关。线粒体肌酸激酶催化肌酸与线粒体中生成的ATP之间的高能磷酸转移。在此过程中生成的磷酸肌酸被转运至肌原纤维。线粒体肌酸激酶异常通过ATP转移紊乱导致细胞质中ATP水平降低。如果这种降低发生在心肌中,则怀疑心脏功能受到抑制。我研究了BIO14.6(肥厚型心肌病模型)在5周、20周、50周和62周龄时以及BIO53.58(扩张型心肌病模型)在5周和20周龄时肌酸激酶系统变化的时间进程。在BIO14.6中,20周、50周和62周龄仓鼠的心肌和分离线粒体的肌酸激酶活性降低。在50周和62周龄仓鼠中,线粒体肌酸激酶在总组织酶活性中的占比降低,而BB型的占比增加。在BIO53.58中,20周龄仓鼠的心肌和分离线粒体的肌酸激酶活性降低。在5周和20周龄仓鼠中,线粒体肌酸激酶的占比增加,而BB型降低。实验表明,BIO14.6在20周龄时以及BIO53.58在新生期发生了肌酸激酶系统的变化。这些肌酸激酶系统的变化可能导致心肌病患者心脏功能受到抑制。