Hong Siting, Zhang Xin, Zhang Xiaohui, Liu Wenxiu, Fu Yu, Liu Yue, Shi Zhiyu, Chi Jinyu, Zhao Meng, Yin Xinhua
Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, Heilongjiang Province, China.
Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, Heilongjiang Province, China.
Biochem Biophys Res Commun. 2017 Jun 3;487(3):728-733. doi: 10.1016/j.bbrc.2017.04.126. Epub 2017 Apr 24.
Calcium sensing receptor (CaSR) mediates pathological cardiac hypertrophy. Mitochondria maintain their function through fission and fusion and disruption of mitochondrial dynamic is linked to various cardiac diseases. This study examined how inhibition of CaSR by the inhibitor Calhex affected the mitochondrial dynamics in a hypertensive model in rats. Spontaneously hypertensive rats (SHRs) and Wistar Kyoto (WKY) rats were used in this study. Cardiac function and blood pressure was evaluated at the end of the study. SHRs showed increases in the ratio of heart weight to body weight and the levels of CaSR; all of these increases were suppressed by Calhex. Additionally, Calhex treatment of SHRs changed the expression of proteins involved in mitochondrial dynamics. Our results demonstrated that CaSR activation induced cardiomyocyte apoptosis through the mitochondrial dynamics mediated apoptotic pathway in hypertensive hearts.
钙敏感受体（CaSR）介导病理性心脏肥大。线粒体通过分裂和融合维持其功能，线粒体动力学的破坏与多种心脏疾病有关。本研究考察了抑制剂Calhex对CaSR的抑制作用如何影响大鼠高血压模型中的线粒体动力学。本研究使用了自发性高血压大鼠（SHRs）和Wistar Kyoto（WKY）大鼠。在研究结束时评估心脏功能和血压。SHRs的心脏重量与体重之比及CaSR水平升高；Calhex抑制了所有这些升高。此外，用Calhex处理SHRs改变了参与线粒体动力学的蛋白质表达。我们的结果表明，CaSR激活通过线粒体动力学介导的凋亡途径诱导高血压心脏中的心肌细胞凋亡。
