心肌肥厚动物模型及代偿机制研究进展
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1.中国医学科学院医学实验动物研究所,北京协和医学院比较医学中心,北京市人类重大疾病实验动物模型工程 技术研究中心,北京 100021; 2.中国医学科学院医学实验动物研究所,北京协和医学院比较医学中心, 国家卫生健康委员会人类疾病比较医学重点实验室,北京 100021

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Research progress on animal models of cardiac hypertrophy and compensation mechanisms
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1.Beijing Engineering Research Center for Experimental Animal Models of Human Diseases, Institute of Laboratory Animal Science, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100021, China. 2. Key Laboratory of Human Disease Comparative Medicine, National Health Commission of China (NHC), Institute of Laboratory Animal Science, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100021

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    摘要:

    心肌肥厚是一种缓慢发展的有效代偿功能,主要发生在长期压力负荷的情况下,是对血流动力学或 心肌损伤的适应性反应,心肌肥厚失代偿最终会增加心力衰竭和猝死的发生率,目前尚无有效的治愈方法。本文就心肌肥厚动物模型,包括小鼠、大鼠及大型动物的制备方法及各自特点,进行总结和比较。 同时对心肌肥厚经典分子信号机制,包括有丝分裂蛋白激酶(MAPKs)信号通路及 Ca2+介导的信号通路等,以及心肌肥厚引发的失代偿分子机制,包括儿茶酚胺及心肌细胞凋亡等信号通路进行的总结和比较。

    Abstract:

    Cardiac hypertrophy is a slow and effective compensatory function that mainly occurs under long-term stress loads. It is an adaptive response to changes in hemodynamics or myocardial injury. Decompensation of myocardial hypertrophy can eventually lead to an increased incidence of heart failure and sudden death, and no effective treatments have been established. In this paper, we summarize and compare the preparation method and characteristics of animal models of cardiac hypertrophy, including mice, rats, and large animals. We also summarize and compare the classical molecular signaling mechanisms of cardiac hypertrophy, including the mitotic protein kinase signaling pathway and the Ca2+ mediated signaling pathway, as well as the molecular mechanisms of decompensation induced by cardiac hypertrophy, including catecholamine and the cardiomyocyte apoptosis signaling pathway.

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刘梦迪,张连峰,吕 丹.心肌肥厚动物模型及代偿机制研究进展[J].中国比较医学杂志,2020,30(8):102~106.

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  • 收稿日期:2020-02-01
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  • 在线发布日期: 2020-09-02
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