钙网蛋白参与诱导线粒体损伤:心肌细胞肥大的新机制

目的观察血管紧张素Ⅱ（AngⅡ）对心肌细胞中钙网蛋白（CRT）表达的影响及其与线粒体功能异常的相关性。方法将
同期原代分离培养的大乳鼠心肌细胞随机分为CRT siRNA组、ctrl siRNA组、对照组、AngⅡ+CRT siRNA组、AngⅡ+ctrl siRNA
组、AngⅡ组，分别测定各组心肌细胞肥大特征、线粒体功能、CRT表达水平的变化。结果与对照组相比，AngⅡ组细胞表面积
及蛋白质合成速率明显升高，线粒体膜电位及呼吸链酶活性降低，同时CRT表达升高。与AngⅡ+ctrl siRNA组相比，AngⅡ+
CRT siRNA组心肌细胞CRT表达明显下调，细胞表面积及蛋白质合成速率明显增加，而线粒体膜电位、呼吸链酶活性降低得到
部分逆转。结论AngⅡ上调心肌细胞CRT表达进而诱导线粒体功能损伤，可能是心肌肥大的重要机制之一。

Calreticulin-induced mitochondrial injury: a novel mechanism of cardiac hypertrophy

Objective To observe the effect of angiotensin II (Ang II) on calreticulin (CRT) expression and its association with
mitochondrial dysfunction in cardiomyocytes. Methods Primary neonatal rat cardiomyocytes were randomly divided into
CRT siRNA group, control siRNA group, control group, Ang II+ CRT siRNA group, Ang II+ control siRNA group and Ang II
group. The cell surface area, protein synthesis rate, mitochondrial membrane potential level, enzyme activities, and CRT
expression were observed. Results Compared with those in the control group, the cell surface area and protein synthesis rate
were both increased and mitochondrial membrane potential level and enzyme activities decreased in Ang II groups. CRT
expression was significantly down-regulated in Ang II+ CRT siRNA group with increased cell surface area, protein synthesis
rate, mitochondrial membrane potential level and enzyme activities as compared with those in Ang II+ control siRNA group.
Conclusion Ang II up-regulates CRT expression to induce mitochondrial injury, which may be an important mechanism of
myocardial hypertrophy.