Role of the calcium sensing receptor in cardiomyocyte apoptosis via mitochondrial dynamics in compensatory hypertrophied myocardium of spontaneously hypertensive rat

Role of the calcium sensing receptor in cardiomyocyte apoptosis via mitochondrial dynamics in compensatory hypertrophied myocardium of spontaneously hypertensive rat
复制标题

钙敏感受体通过线粒体动力学在自发性高血压大鼠代偿性肥大心肌细胞凋亡中的作用

DOI:
10.1016/j.bbrc.2017.04.126
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发表时间:
2017-06-03
影响因子:
3.1
通讯作者:
Yin, Xinhua
Yin, Xinhua
中科院分区:
生物学4区
文献类型:
--
作者:
Hong, Siting;Zhang, Xin;Yin, Xinhua

文献摘要

被引文献

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钙敏感受体(CaSR)介导病理性心肌肥厚。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各种心脏疾病有关。本研究检测了抑制剂Calhex(231)抑制CaSR如何影响大鼠高血压模型中的线粒体动力学。本研究采用自发性高血压大鼠(SHR)和Wistar京都(WKY)大鼠。研究结束时评价心功能和血压。SHR显示心脏重量与体重的比值和CaSR水平增加; Calhex抑制了所有这些增加(231)。此外,Calhex(231)治疗SHR改变了参与线粒体动力学的蛋白质的表达。我们的研究结果表明,在高血压心脏中,CaSR激活通过线粒体动力学介导的凋亡途径诱导心肌细胞凋亡。(C)2017爱思唯尔公司All rights reserved.
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(231) 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(231). Additionally, Calhex(231) 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. (C) 2017 Elsevier Inc. All rights reserved.