TRPC1, CaN and NFATC3 signaling pathway in the pathogenesis and progression of left ventricular hypertrophy in spontaneously hypertensive rats
TRPC1, CaN and NFATC3 signaling pathway in the pathogenesis and progression of left ventricular hypertrophy in spontaneously hypertensive rats
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DOI：
10.3109/10641963.2014.943405
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发表时间：
2015-04
影响因子：
12.3
通讯作者：
Guangrong Zou;Huashan Hong;Xiaohong Lin;Xiaoyun Shi;Ying Wu;Lianglong Chen
中科院分区：
文献类型：
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作者：
Guangrong Zou;Huashan Hong;Xiaohong Lin;Xiaoyun Shi;Ying Wu;Lianglong Chen
摘要采用自发性高血压大鼠（SHR），观察了左室肥厚（LVH）及替米沙坦、氨氯地平干预后LVH的动态变化。结果显示，随着LVH的发生和发展，TRPC 1、CaN和NFATC 3的表达逐渐增强。替米沙坦可降低SHR血压和左室肥厚，下调SHR左室TRPC 1、CaN和NFATC3的表达。黄芪可降低SHR血压，但对心肌肥厚及上述因子的表达无影响。本研究结果提示，SHR LVH的发生、发展与TRPC 1、CaN和NFATC 3信号通路的上调有关。
Abstract Spontaneously hypertensive rats (SHR) was used to study left ventricular hypertrophy (LVH) and its dynamic change after the interventions with Telmisartan and Amlodipine. The results showed that the expression of TRPC1, CaN and NFATC3 increased gradually with the pathogenesis and progression of LVH. Telmisartan reduced blood pressure and LVH, and down-regulated the expression of TRPC1, CaN and NFATC3 in left ventricle of SHR. Amlodipine reduced the blood pressure in SHR but had no impact on the hypertrophy and expression of above factors. Our data suggest that the pathogenesis and progression of LVH in SHR are related to upregulation of TRPC1, CaN and NFATC3 signaling pathway.